Initial renal responses of nonhuman primate to immersion and intravascular volume expansion

1980 ◽  
Vol 48 (2) ◽  
pp. 243-248 ◽  
Author(s):  
T. V. Peterson ◽  
J. P. Gilmore ◽  
I. H. Zucker
Keyword(s):  
Nonhuman Primate ◽  
Volume Expansion ◽  
Diastolic Pressure ◽  
Renal Plasma Flow ◽  
Water Immersion ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Water Excretion ◽  
Arterial Blood ◽  
Renal Responses

Experiments were performed in anesthetized Macaca fascicularis monkeys to determine if the initial renal responses of these animals to head-out vertical water immersion and isoncotic, isotonic volume expansion are similar, especially with regard to the onset of any changes in solute or water excretion. Significant increases in urine flow, sodium excretion, and osmolar clearance occurred after 10 min of immersion but not until 30 min after volume expansion. Potassium excretion increased during immersion but decreased after volume expansion. Mean arterial blood pressure increased after 30 min of immersion but was unchanged after volume expansion. Indices of vascular filling, central venous pressure in the immersed animals and left ventricular end-diastolic pressure in the volume-expanded animals, increased immediately after the intervention. Effective renal plasma flow increased in both groups but glomerular filtration rate was not consistently elevated. These results suggest that, in the nonhuman primate, immersion and volume expansion exert their renal effects through different afferent and/or efferent mechanisms and should not be considered as similar volume stimuli.

Peripheral vascular effects of nitroglycerin in a conscious rat model of heart failure

1982 ◽  
Vol 243 (6) ◽  
pp. H974-H981
Author(s):  
S. F. Flaim
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Diastolic Pressure ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Arterial Blood Flow ◽  
Vascular Effects ◽  
Conscious Rat ◽  
Arterial Blood ◽  
Caudal Artery

The effects of intravenous nitroglycerin (NG; 2, 8, 32 micrograms/kg) on cardiocirculatory dynamics were evaluated in control normal (C) and chronically volume-overloaded [high-output heart failure (aortocaval fistula), HCO] conscious rats. Pressures were recorded in the left ventricle, the caudal artery, and the right atrium. Regional blood flows were determined by radioactive microsphere injection into the left ventricle with reference sampling from the caudal artery. Cardiac output (CO) was 289 ml . min-1 . kg in C and did not change with NG; however, in HCO systemic CO was decreased 31, 23, and 23% by NG from 350 ml . min-1 . kg. In both groups left ventricular end-diastolic pressure was reduced (C, 8.4–5.0; HCO, 19.8–12.7 mmHg); however, central venous pressure was reduced only in C (1.2–0.3 mmHg). During NG primarily at 2 and 8 micrograms/kg, arterial blood flow was lower and vascular resistance was higher in HCO compared with C in the following regions: kidney, ileum, jejunum, skin, heart, spleen, stomach, and testes, whereas no major differences were noted in the cerebellum, cerebrum, liver, or skeletal muscle. Thus acute NG infusion is a more potent regional vasodilator in C than in HCO. It is suggested that this difference is related to a more powerful NG-induced sympathetic reflex activation in the HCO group, which strongly attenuates the direct vasodilator effect of NG that was apparent in C.

Increased ANF secretion after volume expansion is preserved in rats with heart failure

1988 ◽  
Vol 254 (2) ◽  
pp. R185-R191 ◽  
Author(s):  
Y. W. Chien ◽  
R. W. Barbee ◽  
A. A. MacPhee ◽  
E. D. Frohlich ◽  
N. C. Trippodo
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Blood Volume ◽  
Volume Expansion ◽  
Diastolic Pressure ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Blood Volume Expansion

To examine whether the failing heart has reached a maximal capacity to increase plasma atrial natriuretic factor (ANF) concentration, the change in plasma immunoreactive ANF level due to acute blood volume expansion was determined in conscious rats with chronic heart failure. Varying degrees of myocardial infarction and thus heart failure were induced by coronary artery ligation 3 wk before study. Compared with controls, infarcted rats had decreases in mean arterial pressure (-10 mmHg, P less than 0.01), cardiac index (-27%, P less than 0.001), renal blood flow (-35%, P less than 0.01), and peak left ventricle-developed pressure after aortic occlusion (an index of pressure generating ability; -15%, P less than 0.01), and increases in central venous pressure (+1.7 mmHg, P less than 0.01), left ventricular end-diastolic pressure (+10 mmHg, P less than 0.001), total peripheral resistance (+28%, P less than 0.01), and plasma ANF level (752 +/- 109 vs. 244 +/- 33 pg/ml, P less than 0.001). Plasma ANF was correlated with infarct size, cardiac filling pressures, and left ventricle pressure-generating ability. At 5 min after 25% blood volume expansion, plasma ANF in rats with heart failure increased by 2,281 +/- 345 pg/ml; the magnitude of the changes in circulating ANF and hemodynamic measurements was similar in controls. The results suggest that plasma ANF level can be used as a reliable index of the severity of heart failure, and that the capacity to increase plasma ANF concentration after acute volume expansion is preserved in rats with heart failure. There was no evidence of a relative deficiency of circulating ANF in this model of heart failure.

Pregnant rats are refractory to the natriuretic actions of atrial natriuretic peptide

1994 ◽  
Vol 267 (6) ◽  
pp. R1611-R1616 ◽  
Author(s):  
S. Masilamani ◽  
L. Castro ◽  
C. Baylis
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Volume Expansion ◽  
Renal Plasma Flow ◽  
Pregnant Rats ◽  
Arterial Blood ◽  
Renal Vascular ◽  
Renal Responses ◽  
Percent Decline ◽  
Atrial Natriuretic

Normal pregnant women and rats undergo a volume expansion. Atrial natriuretic peptide (ANP) is involved in volume homeostasis and is stimulated in response to volume expansion in nonpregnant animals, resulting in natriuresis and diuresis. The conscious, chronically catheterized rat was used to measure mean arterial blood pressure (MABP) and renal responses to administered ANP (160 ng.kg-1.min-1 i.v.) to determine if the actions of ANP are altered by pregnancy. These experiments examined virgin (n = 7) and pregnant rats, studied on gestational days 7-9 (n = 9) and 15-17 (n = 7). Renal clearance studies (with inulin and p-aminohippurate) were conducted in control conditions and during 60 min of ANP infusion. After the ANP infusion, plasma ANP concentrations were measured in virgin and pregnant rats. MABP fell with ANP infusion to similar absolute values in virgins (112 +/- 2 to 80 +/- 6 mmHg), 7- to 9-day pregnant (114 +/- 2 to 91 +/- 3 mmHg), and 15- to 17-day pregnant (107 +/- 2 to 88 +/- 4 mmHg) rats although the percent decline in MABP in 15- to 17-day pregnant rats was less than in virgins. Plasma ANP concentrations were similar in all groups. ANP had no effect on glomerular filtration rate, renal plasma flow, or renal vascular resistance in virgin or pregnant rats. ANP increased sodium excretion in virgins and in 7- to 9-day pregnant rats (+102 +/- 27 and +135 +/- 47%, respectively) but not in 15- to 17-day pregnant animals (+23 +/- 22%).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals AT II Receptor Blockade and Renal Denervation: Different Interventions with Comparable Renal Effects?

2021 ◽  
pp. 1-11
Author(s):  
Kristina Rodionova ◽  
Martin Hindermann ◽  
Karl Hilgers ◽  
Christian Ott ◽  
Roland E. Schmieder ◽  
...  
Keyword(s):  
Body Weight ◽  
Volume Expansion ◽  
Neural Control ◽  
Renal Denervation ◽  
Urine Volume ◽  
Receptor Blockade ◽  
Ang Ii ◽  
Water Excretion ◽  
Arterial Blood ◽  
Renal Sympathetic

<b><i>Background:</i></b> Angiotensin II (Ang II) and the renal sympathetic nervous system exert a strong influence on renal sodium and water excretion. We tested the hypothesis that already low doses of an Ang II inhibitor (candesartan) will result in similar effects on tubular sodium and water reabsorption in congestive heart failure (CHF) as seen after renal denervation (DNX). <b><i>Methods:</i></b> Measurement of arterial blood pressure, heart rate (HR), renal sympathetic nerve activity (RSNA), glomerular filtration rate (GFR), renal plasma flow (RPF), urine volume, and urinary sodium. To assess neural control of volume homeostasis, 21 days after the induction of CHF via myocardial infarction rats underwent volume expansion (0.9% NaCL; 10% body weight) to decrease RSNA. CHF rat and controls with or without DNX or pretreated with the Ang II type-1 receptor antagonist candesartan (0.5 ug i.v.) were studied. <b><i>Results:</i></b> CHF rats excreted only 68 + 10.2% of the volume load (10% body weight) in 90 min. CHF rats pretreated with candesartan or after DNX excreted from 92 to 103% like controls. Decreases of RSNA induced by volume expansion were impaired in CHF rats but unaffected by candesartan pointing to an intrarenal drug effect. GFR and RPF were not significantly different in controls or CHF. <b><i>Conclusion:</i></b> The prominent function of increased RSNA – retaining salt and water – could no longer be observed after renal Ang II receptor blockade in CHF rats.

DNA enzyme targeting TNF-α mRNA improves hemodynamic performance in rats with postinfarction heart failure

2001 ◽  
Vol 281 (5) ◽  
pp. H2211-H2217 ◽  
Author(s):  
Per Ole Iversen ◽  
Gunnar Nicolaysen ◽  
Mouldy Sioud
Keyword(s):  
Heart Failure ◽  
Therapeutic Potential ◽  
Diastolic Pressure ◽  
Substantial Reduction ◽  
Left Ventricular ◽  
Lung Weight ◽  
Cleavage Activity ◽  
Arterial Blood ◽  
Modified Dna ◽  
Tnf Α

Tumor necrosis factor-α (TNF-α) probably affects the pathogenesis of heart failure. Here we have investigated the therapeutic potential of a nuclease-resistant DNA enzyme that specifically cleaves TNF-α mRNA. A phosphorothioate-modified DNA enzyme was designed to retain similar cleavage activity as its unmodified version, and that inhibited the expression of TNF-α in vitro. To test its efficacy in vivo, postinfarction congestive heart failure was induced in anesthetized rats by ligation of the left coronary artery. A 4-wk treatment with the DNA enzyme induced a substantial reduction in left ventricular end-diastolic pressure and lung weight concomitant with an increase in arterial blood pressure and myocardial blood flow compared with controls. The concentration of TNF-α in coronary sinus blood was markedly lowered on treatment, and myocardial TNF-α mRNA was substantially reduced. Recovery studies showed that the DNA enzyme cleavage activity was present within the myocardium throughout the observation period and had no apparent toxic effects. Our findings indicate that DNA enzyme-based therapy may hold promise in the treatment of this debilitating disease.

Cardiovascular and renal effects of hypoxia in conscious carotid body-denervated rats

1993 ◽  
Vol 74 (6) ◽  
pp. 2795-2800 ◽  
Author(s):  
R. Behm ◽  
H. Mewes ◽  
W. H. DeMuinck Keizer ◽  
T. Unger ◽  
R. Rettig
Keyword(s):  
Carotid Body ◽  
Normobaric Hypoxia ◽  
Sodium Potassium ◽  
Water Excretion ◽  
Excretory Function ◽  
Arterial Blood ◽  
Peripheral Arterial ◽  
Renal Responses ◽  
Arterial Po2 ◽  
Sodium And Potassium

The contribution of peripheral arterial chemoreceptors to cardiovascular and renal responses to acute hypocapnic hypoxia is currently not well understood. We compared the effects of normobaric hypoxia on mean arterial blood pressure (MABP), heart rate, glomerular filtration rate (GFR), renal blood flow (RBF), and renal volume and electrolyte excretion in conscious unilaterally nephrectomized carotid body-denervated (n = 10) and sham-operated (n = 10) control rats. Thirty minutes of normobaric hypoxia (12.5% O2) resulted in significant reductions in arterial PO2 and PCO2 as well as decreases in MABP, GFR, RBF, and renal sodium, potassium, and water excretion. These effects occurred more rapidly and/or were significantly more pronounced in carotid body-denervated than in sham-operated rats. These data indicate that moderate acute hypocapnic hypoxia has profound effects on systemic and renal hemodynamics as well as on renal excretory function in conscious rats. We conclude that stimulation of the peripheral arterial chemoreceptors can partially offset the hypoxia-induced decreases in MABP, RBF, GFR, urine flow, and urinary sodium and potassium excretion, thereby helping to maintain cardiovascular as well as fluid and electrolyte homeostasis.

Contribution of abdomen and legs to central blood volume expansion in humans during immersion

1997 ◽  
Vol 83 (3) ◽  
pp. 695-699 ◽  
Author(s):  
Lars Bo Johansen ◽  
Thomas Ulrik Skram Jensen ◽  
Bettina Pump ◽  
Peter Norsk
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Protein Concentration ◽  
Water Immersion ◽  
Venous Pressure ◽  
Cuff Inflation ◽  
Central Blood Volume ◽  
Central Venous ◽  
Plasma Protein Concentration ◽  
Blood Volume Expansion

Johansen, Lars Bo, Thomas Ulrik Skram Jensen, Bettina Pump, and Peter Norsk. Contribution of abdomen and legs to central blood volume expansion in humans during immersion. J. Appl. Physiol. 83(3): 695–699, 1997.—The hypothesis was tested that the abdominal area constitutes an important reservoir for central blood volume expansion (CBVE) during water immersion in humans. Six men underwent 1) water immersion for 30 min (WI), 2) water immersion for 30 min with thigh cuff inflation (250 mmHg) during initial 15 min to exclude legs from contributing to CBVE (WI+Occl), and 3) a seated nonimmersed control with 15 min of thigh cuff inflation (Occl). Plasma protein concentration and hematocrit decreased from 68 ± 1 to 64 ± 1 g/l and from 46.7 ± 0.3 to 45.5 ± 0.4% ( P < 0.05), respectively, during WI but were unchanged during WI+Occl. Left atrial diameter increased from 27 ± 2 to 36 ± 1 mm ( P < 0.05) during WI and increased similarly during WI+Occl from 27 ± 2 to 35 ± 1 mm ( P < 0.05). Central venous pressure increased from −3.7 ± 1.0 to 10.4 ± 0.8 mmHg during WI ( P < 0.05) but only increased to 7.0 ± 0.8 mmHg during WI+Occl ( P < 0.05). In conclusion, the dilution of blood induced by WI to the neck is caused by fluid from the legs, whereas the CBVE is caused mainly by blood from the abdomen.

scholarly journals Possible mechanism of the cardio-renal protective effects of AVE-0991, a non-peptide Mas-receptor agonist, in diabetic rats

2012 ◽  
Vol 13 (3) ◽  
pp. 334-340 ◽  
Author(s):  
Kulwinder Singh ◽  
Kuldeepak Sharma ◽  
Manjeet Singh ◽  
PL Sharma
Keyword(s):  
Blood Pressure ◽  
Receptor Agonist ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Protective Effects ◽  
Mas Receptor ◽  
Arterial Blood

Hypothesis: This study was designed to investigate the cardio-renal protective effect of AVE-0991, a non-peptide Mas-receptor agonist, and A-779, a Mas-receptor antagonist, in diabetic rats. Materials and methods: Wistar rats treated with streptozotocin (50 mg/kg, i.p., once), developed diabetes mellitus after 1 week. After 8 weeks, myocardial functions were assessed by measuring left ventricular developed pressure (LVDP), rate of left ventricular pressure development (d p/d tmax), rate of left ventricular pressure decay (d p/d tmin) and left ventricular end diastolic pressure (LVEDP) on an isolated Langendorff’s heart preparation. Further, mean arterial blood pressure (MABP) was measured by using the tail-cuff method. Assessment of renal functions and lipid profile was carried out using a spectrophotometer. Results: The administration of streptozotocin to rats produced persistent hyperglycaemia, dyslipidaemia and hypertension which consequently produced cardiac and renal dysfunction in 8 weeks. AVE0991 treatment produced cardio-renal protective effects, as evidenced by a significant increase in LVDP, d p/d tmax, d p/d tmin and a significant decrease in LVEDP, BUN, and protein urea. Further, AVE-0991 treatment for the first time has been shown to reduce dyslipidaemia and produced antihyperglycaemic activity in streptozotocin-treated rats. However, MABP and creatinine clearance remained unaffected with AVE-0991 treatment. Conclusions: AVE-0991 produced cardio-renal protection possibly by improving glucose and lipid metabolism in diabetic rats, independent of its blood pressure lowering action.

Vasopressin potentiates ventricular and arterial reflexes in the conscious nonhuman primate

1989 ◽  
Vol 256 (6) ◽  
pp. H1546-H1552 ◽  
Author(s):  
M. W. Barazanji ◽  
K. G. Cornish
Keyword(s):  
Blood Pressure ◽  
Nonhuman Primate ◽  
Nucleus Tractus Solitarius ◽  
Control Level ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Rule Out

The effect of arginine vasopressin (AVP) on the arterial baroreflex control of heart rate (HR) was studied in intact and sinoaortic-denervated (SAD) conscious, unrestrained monkeys. A baroreflex curve for mean arterial blood pressure (MABP) and HR was determined before and during intravenous infusion of AVP (2-4 mU.kg-1.min-1) and after the AVP vascular antagonist "Manning compound" [( d(CH2)5Tyr(Me)]AVP, 40 micrograms/kg), while AVP infusion was kept running. The sensitivity (slope) of the arterial baroreflex, as well as the reflex bradycardia induced by high blood pressure, increased significantly during AVP and returned to the control level after Manning compound. The effect of AVP on the Bezold-Jarisch reflex (induced by stimulating left ventricular receptors with 4 micrograms/kg veratridine injected in the left atrium) was also studied. The cardiovascular responses to veratridine were examined before and during AVP and after administration of Manning compound together with AVP infusion. AVP significantly potentiated the hypotension and the bradycardia produced by veratridine, whereas Manning compound blunted this potentiation. The ventricular reflex in SAD monkeys was significantly greater than in intact monkeys. We conclude that, in the conscious nonhuman primate, AVP potentiates the sensitivity of the baroreflex control of HR as well as the Bezold-Jarisch reflex. The potentiation of the Bezold-Jarisch reflex by AVP in the SAD animals is consistent with a central action, since the baroreceptors and ventricular receptors both have connections in the nucleus tractus solitarius. However, it does not rule out the possibility of peripheral actions on receptors or end organs.

Positive end-expiratory pressure shifts left ventricular diastolic pressure-area curves

1980 ◽  
Vol 48 (4) ◽  
pp. 670-676 ◽  
Author(s):  
J. B. Haynes ◽  
S. D. Carson ◽  
W. P. Whitney ◽  
G. O. Zerbe ◽  
T. M. Hyers ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Volume Expansion ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Positive End Expiratory Pressure ◽  
Pressure Area ◽  
Radiopaque Markers ◽  
Peep Ventilation ◽  
Volume Characteristics ◽  
Area Data

Positive end-expiratory pressure (PEEP) ventilation is frequently associated with reduction in cardiac output despite unchanged transmural left ventricular (LV) end-diastolic pressure. These findings have been interpreted to indicate decreased contractility, but could also be explained by altered LV diastolic pressure-volume characteristics. To study this possibility, radiopaque markers were inserted into a plane of the LV in nine dogs. Transmural pressure (LV-pericardial) was synchronized with LV area during ventilation with zero end-expiratory pressure and with 15 cmH2O PEEP. Mean polynomial curves derived from the diastolic pressure-area data demonstrated that PEEP shifted the curves upward so that a given diastolic area was associated with a higher transmural LV pressure (P less than 0.0001). PEEP decreased end-diastolic area and stroke area, both of which were normalized with dextran volume expansion. Restoration of stroke area by normalizing end-diastolic area with volume expansion suggests the initial changes with PEEP were due to a decrease in preload rather than in contractility.

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