Increase in sympathetic activity with age. II. Role of impairment of cardiopulmonary baroreflexes

1991 ◽  
Vol 260 (4) ◽  
pp. H1121-H1127 ◽  
Author(s):  
G. Hajduczok ◽  
M. W. Chapleau ◽  
F. M. Abboud

We have previously shown that arterial baroreflex function is significantly impaired in a group of old beagles [G. Hajduczok, M. W. Chapleau, S. L. Johnson, and F. M. Abboud. Am. J. Physiol. 260 (Heart Circ. Physiol. 29): H1113-H1120, 1991]. In the present study, we determined whether the neural limb of the cardiopulmonary baroreflex control of renal sympathetic nerve activity (RSNA) and the interaction between the arterial and cardiopulmonary reflexes is also impaired with senescence. In the anesthetized state, the aortic nerves were sectioned and carotid sinuses were isolated bilaterally with carotid sinus pressures held at 50 mmHg in both young (1 yr) and old animals (11 yr). In response to graded volume expansion (VE) with 3% dextran (0 to 30 ml/kg iv), the gain of cardiopulmonary baroreflex control of RSNA was significantly lower in the old (5.1 +/- 3%/mmHg) compared with the young (13.4 +/- 3%/mmHg) animals. There were no significant differences in systemic vascular compliance or left ventricular mass index between the two groups. The gain of the carotid sinus baroreflex inhibition of RSNA was significantly attenuated by VE in the young group but was not affected in the old group. Bilateral vagotomy (VX) resulted in a 182 +/- 74% increase in RSNA in the young (P less than 0.05), but VX did not significantly increase RSNA in the old (12 +/- 17%). After VX, the carotid sinus baroreflex gain markedly increased by nearly eightfold in the young group (P less than 0.05) but was not altered in the old dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

1991 ◽  
Vol 260 (4) ◽  
pp. H1113-H1120 ◽  
Author(s):  
G. Hajduczok ◽  
M. W. Chapleau ◽  
S. L. Johnson ◽  
F. M. Abboud

The purpose of this study was to evaluate changes in arterial baroreflex function with aging. Mean arterial pressure (MAP) obtained in the awake state was 110 +/- 7 mmHg in the young animals (1 yr; n = 5) and 128 +/- 6 mmHg in the old beagles (11 yr; n = 11) (P less than 0.05). In response to bolus administration of varying doses of phenylephrine and nitroglycerin in the conscious state, the slope relating heart rate (HR) to MAP was attenuated significantly in the old animals compared with the young (-0.87 +/- 0.30 vs. -2.35 +/- 0.44 beats.min-1.mmHg-1; P less than 0.05). After atropine, the baroreflex control of HR was abolished in both groups. After anesthesia and sectioning of the aortic depressor nerves, and with isolated carotid sinus pressures (CSP) held at 50 mmHg, absolute renal sympathetic nerve activity (RSNA) was significantly greater in the old (368 +/- 40 Hz) vs. the young animals (41 +/- 9 Hz). In the old, the gains of baroreflex inhibition of MAP (0.78 +/- 0.09) and normalized RSNA (0.38 +/- 0.14%/mmHg) during increases in CSP were decreased significantly compared with the young (MAP, 1.16 +/- 0.17 mmHg, and RSNA, 0.72 +/- 0.06%/mmHg). In a subgroup of old normotensive animals (n = 5), the baroreflex gain of RSNA was still attenuated (0.43 +/- 0.11%/mmHg) compared with the young. The reflex reduction in absolute RSNA as a function of baseline RSNA was also impaired in old vs. young beagles.(ABSTRACT TRUNCATED AT 250 WORDS)


1993 ◽  
Vol 264 (4) ◽  
pp. H1215-H1222 ◽  
Author(s):  
L. Hayward ◽  
M. Hay ◽  
R. B. Felder

The effect of prolonged aortic depressor nerve (ADN) stimulation on carotid sinus baroreflex regulation of arterial pressure (AP) and renal sympathetic nerve activity (RSNA) was examined in anesthetized rabbits. Ramp increases in carotid sinus pressure (CSP) were repeated before and after 5 min of bilateral ADN stimulation. One minute after ADN stimulation the curve relating AP to CSP had shifted up and to the right, characterized by significant increases (P < 0.05) in the maximum (91 +/- 2 to 101 +/- 3 mmHg; mean +/- SE), midpoint (118 +/- 7 to 125 +/- 8 mmHg CSP), and minimum (45 +/- 3 to 53 +/- 4 mmHg) of the AP reflex curve. There was a parallel shift downward of the curve relating RSNA to CSP, characterized by significant decreases in the maximum [100 +/- 0 to 66 +/- 8% of maximum control RSNA value (%max)], the range (90 +/- 2 to 59 +/- 8%max), and the gain (-1.0 +/- 0.2 to -0.5 +/- 0.1%max/mmHg) of the RSNA reflex curve. Values returned to control within 10 min of cessation of ADN stimulation. These results suggest that central neurons processing baroreflex information from one set of mechanoreceptors can be reset by convergent signals arising from another baroreceptor site.


2001 ◽  
Vol 280 (5) ◽  
pp. H1996-H2005 ◽  
Author(s):  
Kathleen P. O'Hagan ◽  
Kara A. Skogg ◽  
Jennifer B. Stevenson

The role of ANG II in the arterial baroreflex control of renal sympathetic nerve activity (RSNA) in eight term-pregnant (P) and eight nonpregnant (NP) conscious rabbits was assessed using sequential intracerebroventricular and intravenous infusions of losartan, an AT1 receptor antagonist. The blood pressure (BP)-RSNA relationship was generated by sequential inflations of aortic and vena caval perivascular occluders. Pregnant rabbits exhibited a lower maximal RSNA reflex gain (−44%) that was primarily due to a reduction in the maximal sympathetic response to hypotension (P, 248 ± 20% vs. NP, 357 ± 41% of rest RSNA, P < 0.05). Intracerebroventricular losartan decreased resting BP in P (by 9 ± 3 mmHg, P < 0.05) but not NP rabbits, and had no effect on the RSNA baroreflex in either group. Subsequent intravenous losartan decreased resting BP in NP and further decreased BP in P rabbits, but had no significant effect on the maximal RSNA reflex gain. ANG II may have an enhanced role in the tonic support of BP in pregnancy, but does not mediate the gestational depression in the arterial baroreflex control of RSNA in rabbits.


1992 ◽  
Vol 263 (6) ◽  
pp. R1187-R1194 ◽  
Author(s):  
Y. Nishida ◽  
V. S. Bishop

We tested the hypothesis that the inhibitory action of arginine vasopressin (AVP) on renal sympathetic nerve activity (RSNA) is related to the number of baroreceptor stations. The role of baroreceptor afferents was determined by comparing the effects of AVP on the baroreflex function curves [mean arterial pressure (MAP) vs. %RSNA] obtained in intact conscious rabbits with those obtained in rabbits with one carotid sinus and one aortic nerve intact (1CSN + 1AoN) and in rabbits with only a single carotid sinus nerve intact (1CSN). Baroreflex curves were obtained by relating %RSNA to MAP during ramp increases and decreases in MAP. MAP was increased with phenylephrine and decreased with caval occlusion. In the intact state (n = 7), AVP infusions (0.4, 1.5, and 3.0 mU.kg-1 x min-1) produced dose-dependent reduction in the maximum %RSNA (97 +/- 1 to 85 +/- 6, 68 +/- 6, and 57 +/- 5%, respectively) at minimum MAP and the gain of the baroreflex curve (5.7 +/- 0.2 to 3.9 +/- 0.2, 3.2 +/- 0.3, and 2.2 +/- 0.2 mmHg, respectively) and shifted the midrange of the curves (72 +/- 3 to 68 +/- 4, 68 +/- 2, and 63 +/- 3 mmHg, respectively). However, in the 1CSN + 1AoN state (n = 6), the medium dose of AVP (1.5 mU.kg-1 x min-1) did not significantly alter the maximum %RSNA, the gain of the curve, or the midrange of the curve. The highest dose of AVP (3.0 mU.kg-1 x min-1) still reduced the maximum %RSNA (98 +/- 3 to 75 +/- 3) and the gain of the curve (4.1 +/- 0.4 to 2.7 +/- 0.2).(ABSTRACT TRUNCATED AT 250 WORDS)


1995 ◽  
Vol 268 (1) ◽  
pp. H61-H67 ◽  
Author(s):  
B. S. Huang ◽  
F. H. Leenen

In young Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) with or without chronic sinoaortic denervation (SAD), we evaluated the effects of low, regular, and high dietary sodium intake (L-Na, R-Na, and H-Na, respectively) from 4 to 8 wk of age on cardiopulmonary baroreflex function, which was assessed by changes in renal sympathetic nerve activity (RSNA) and heart rate (HR) in response to acute volume expansion. In intact SHR H-Na increased blood pressure (BP), whereas L-Na decreased BP. No changes were observed in intact WKY. The gain of the cardiopulmonary baroreflex control of both HR and RSNA was significantly attenuated in SHR vs. WKY on R-Na. In both SHR and WKY, L-Na had no effects on the gain of RSNA and HR responses. In both strains, H-Na did not affect the gain of HR but attenuated the gain of the RSNA response. H-Na attenuated the gain of RSNA response more in SHR with SAD vs. intact SHR (52 vs. 69% of corresponding R-Na control) but less in WKY with SAD vs. intact WKY (80 vs. 71% of corresponding R-Na control). These data indicate that in SHR, H-Na further desensitizes the already impaired cardiopulmonary baroreflex control of RSNA. After SAD, this attenuation is more prominent in SHR but becomes less prominent in WKY. High sodium intake, therefore, modulates the interaction between the arterial and cardiopulmonary baroreflexes in the control of RSNA oppositely in WKY vs. SHR.


2001 ◽  
Vol 280 (3) ◽  
pp. R646-R654 ◽  
Author(s):  
Jeffrey L. Segar ◽  
Kurt A. Bedell ◽  
Oliva J. Smith

The mechanisms by which antenatal glucocorticoids facilitate postnatal circulatory function in preterm infants are uncertain but may be related to augmented angiotensinergic functions. To test the hypothesis that the effects of glucocorticoids on postnatal cardiovascular and sympathetic activity are mediated via the renin-angiotensin system, we studied the effects of AT1 receptor blockade on postnatal changes in heart rate (HR), mean arterial blood pressure (MABP), renal sympathetic nerve activity (RSNA), and baroreflex control of HR in prematurely delivered lambs. After maternal administration of betamethasone (12 mg im 48 and 24 h before delivery), chronically instrumented preterm lambs (118- to 123-day gestation, term 145 days) were studied before and after delivery by cesarean section; fetuses received either the AT1 receptor antagonist losartan (10 mg iv, n = 6) or saline ( n = 6) 1 h before delivery. A third group of animals ( n = 6) received losartan without prior exposure to betamethasone. Compared with fetal values, betamethasone-treated animals demonstrated significant increases ( P < 0.05) in MABP (47 ± 2 to 58 ± 2 mmHg) and RSNA (181 ± 80% of fetal value) 1 h after delivery. Betamethasone + losartan-treated lambs also displayed increases in MABP (48 ± 1 to 55 ± 3 mmHg) and RSNA (198 ± 96% of fetal value) 60 min after birth, similar to betamethasone alone lambs. Losartan alone treated animals had no postnatal increase in either MABP or RSNA, responses similar to those seen in nontreated sheep delivered at the same gestational age. The sensitivity of baroreflex-mediated changes in HR in response to increases in MABP was less in both groups of betamethasone-treated animals; no effect was seen with losartan. These results suggest the postnatal increases in MABP and RSNA seen with antenatal glucocorticoid treatment are not mediated by stimulation of peripherally accessible AT1 receptors. We speculate that augmented cardiovascular function in glucocorticoid-treated premature lambs is dependent, in part, on a generalized sympathoexcitatory response and that this effect of glucocorticoids is mediated by central mechanisms.


1996 ◽  
Vol 270 (3) ◽  
pp. H988-H1000 ◽  
Author(s):  
J. T. Potts ◽  
T. Hatanaka ◽  
A. A. Shoukas

Capacitive properties of the arterial and venous segments of the peripheral circulation are important in the regulation of cardiac output and arterial blood pressure. We examined whether an acute increase in arterial compliance C(a) would alter carotid sinus baroreflex control of the circulation. Eight mongrel dogs were anesthetized with pentobarbital sodium, and the carotid sinus regions were isolated and perfused with nonpulsatile pressures. Open-loop baroreflex response curves for systemic arterial pressure (SAP), heart rate (HR), aortic blood flow (ABF), peripheral vascular resistance (PVR), and left ventricular (LV) contractility were obtained when carotid sinus pressure (CSP) was changed in 25-mmHg steps between 50 and 200 mmHg under a control condition and when C(a) was increased by including two hydraulic compliant chambers to the arterial circulation (CS 1.72 ml/mmHg and CL 5.05 ml/mmHg). The compliant chambers significantly increased C(a) and altered the ratio of arterial to venous compliance C(a)/Cv). Changes in C(a)/Cv significantly decreased the maximal open-loop baroreflex gain (Gmax) for SAP (-2.3 +/- 0.5, -1.6 +/- 0.3, and -1.1 +/- 0.2 mmHg/mmHg, control vs. CS vs. CL, P < 0.05). Gmax for ABF was decreased by CS (-0.9 +/- 0.2 vs. -0.3 +/- 0.1 ml.kg-1.min-1, control vs. CS, P < 0.05), and CL reversed the reflex changes in ABF (Gmax: +0.6 +/- 0.3 ml.kg-1.min-1). Gmax for HR, PVR, and LV contractility was not altered when C(a) was increased (P > 0.05). These findings indicate that an increase in C(a) changes C(a)/Cv and alters carotid baroreflex control of SAP by modifying the ABF response. We conclude that a change in C(a)/Cv affects the reflex control of the circulation by altering the distribution of blood volume between the arterial and venous circulations.


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