Effects of long-term blockade of angiotensin converting enzyme with captopril on blood pressure and aortic prolyl hydroxylase activity in spontaneously hypertensive rats

1983 ◽  
Vol 91 (2-3) ◽  
pp. 283-286 ◽  
Author(s):  
Takeshi Oshima ◽  
Youchi Matsushita ◽  
Masaaki Miyamoto ◽  
Hiroyuki Koike
Keyword(s):  
Blood Pressure ◽  
Angiotensin Converting Enzyme ◽  
Spontaneously Hypertensive Rats ◽  
Prolyl Hydroxylase ◽  
Converting Enzyme ◽  
Hypertensive Rats ◽  
Hydroxylase Activity ◽  
Spontaneously Hypertensive

Effects of benazepril, an angiotensin-converting enzyme inhibitor, combined with CGS 35066, a selective endothelin-converting enzyme inhibitor, on arterial blood pressure in normotensive and spontaneously hypertensive rats

2002 ◽  
Vol 103 (s2002) ◽  
pp. 363S-366S ◽  
Author(s):  
Bruno BATTISTINI ◽  
Bilal AYACH ◽  
Stéphanie MOLEZ ◽  
Andre BLOUIN ◽  
Arco Y. JENG
Keyword(s):  
Blood Pressure ◽  
Angiotensin Converting Enzyme ◽  
Spontaneously Hypertensive Rats ◽  
Ace Inhibitor ◽  
Enzyme Inhibitor ◽  
Converting Enzyme ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Arterial Blood ◽  
Endothelin Converting Enzyme

Continuous intra-arterial administration of a selective endothelin-converting enzyme (ECE) inhibitor CGS 35066 at a dose of 30mg/kg decreased the mean arterial blood pressure (MABP) in conscious unrestrained normotensive rats and spontaneously hypertensive rats (SHRs). At that dose, the magnitude of the antihypertensive effects was greater in SHRs than in normotensive rats. Additional administration of an angiotensin-converting enzyme (ACE) inhibitor benazapril (lotensin) further reduced MABP in normotensive rats and completely blocked hypertension in SHRs. However, when the selective ECE inhibitor was subsequently removed, blood pressure was less inhibited in normotenive rats whereas it remained strongly inhibited in SHRs by the ACE inhibitor alone. These results imply that simultaneous treatment with benazepril and CGS 35066 gave additive antihypertensive effects in normotensive rats but not in SHRs, when both compounds were administered at a dose of 30mg/kg. Our results suggest that: (i) the endothelin (ET) system together with the renin–angiotensin system contribute to the maintenance of blood pressure in normal healthy rats; (ii) while an ECE inhibitor acts as an antihypertensive agent on its own, the sole efficacy of ACE inhibitor at that dose is sufficient to block MABP without the participation of the ET system in SHR.

scholarly journals Angiotensin II Inhibition Reduces Stress Sensitivity of Hypothalamo-Pituitary-Adrenal Axis in Spontaneously Hypertensive Rats

Endocrinology ◽  
2006 ◽  
Vol 147 (7) ◽  
pp. 3539-3546 ◽  
Author(s):  
Walter Raasch ◽  
Christian Wittmershaus ◽  
Andreas Dendorfer ◽  
Inga Voges ◽  
Friedrich Pahlke ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Hpa Axis ◽  
Spontaneously Hypertensive Rats ◽  
Converting Enzyme ◽  
Hypertensive Rats ◽  
At1 Receptors ◽  
Spontaneously Hypertensive ◽  
Baseline Levels

Angiotensin II type 1 (AT1) receptors are expressed within organs of the hypothalamo-pituitary-adrenal (HPA) axis and seem to be important for its stress responsiveness. Secretion of CRH, ACTH, and corticosterone (CORT) is increased by stimulation of AT1 receptors. In the present study, we tested whether a blockade of the angiotensin II system attenuates the HPA axis reactivity in spontaneously hypertensive rats. Spontaneously hypertensive rats were treated with candesartan (2 mg/kg), ramipril (1 mg/kg), or mibefradil (12 mg/kg) for 5 wk. In addition to baseline levels, CORT and ACTH responses to injection of CRH (100 μg/kg) were monitored over 4 h. mRNA of CRH, proopiomelanocortin, AT1A, AT1B, and AT2 receptors was quantified by real-time PCR. All treatments induced equivalent reductions of blood pressure and had no effect on baseline levels of CORT and ACTH. However, both candesartan and ramipril significantly reduced CRH-stimulated plasma levels of ACTH (−26 and −15%) and CORT (−36 and −18%) and lowered hypothalamic CRH mRNA (−25 and −29%). Mibefradil did not affect any of these parameters. Gene expression of AT1A, AT1B, and AT2 receptors within the HPA axis was not altered by any drug. We show for the first time that antihypertensive treatment by inhibition of AT1 receptors or angiotensin-converting enzyme attenuates HPA axis reactivity independently of blood pressure reduction. This action is solely evident after CRH stimulation but not under baseline conditions. Both a reduced pituitary sensitivity to CRH and a down-regulation of hypothalamic CRH expression have the potential to reduce HPA axis activity during chronic AT1 blockade or angiotensin-converting enzyme inhibition.

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