Abstract
We investigated the effects of losartan, an AT1-receptor blocker, and ramipril, a converting enzyme inhibitor, on the pressor response induced by angiotensin II (ANG II) and carbachol (a cholinergic receptor agonist). Male Holtzman rats (250-300 g) with a stainless steel cannula implanted into the lateral ventricle (LV) were used. The injection of losartan (50 nmol/1 microliter) into the LV blocked the pressor response induced by ANG II (12 ng/1 microliter) and carbachol (2 nmol/1 microliter). After injection of ANG II and carbachol into the LV, mean arterial pressure (MAP) increased to 31 +/- 1 and 28 +/- 2 mmHg, respectively. Previous injection of losartan abolished the increase in MAP induced by ANG II and carbachol into the LV (2 +/- 1 and 5 +/- 2 mmHg, respectively). The injection of ramipril (12 ng/1 microliter) prior to carbachol blocked the pressor effect of carbachol to 7 +/- 3 mmHg. These results suggest an interaction between central cholinergic pathways and the angiotensinergic system in the regulation of arterial blood pressure.
Highlights
Presented at the International Symposium Neuroendocrine Control of Body Fluid Homeostasis, Ribeirão Preto, SP, Brasil, August 17-20, 1996
We investigated the effects of losartan, an AT1-receptor blocker, and ramipril, a converting enzyme inhibitor, on the pressor response induced by angiotensin II (ANG II) and carbachol
In order to confirm whether the pressor response to central injection of carbachol implicates the reninangiotensin system we utilized the converting enzyme inhibitor ramipril to study its effects on the pressor response to carbachol
Summary
Presented at the International Symposium Neuroendocrine Control of Body Fluid Homeostasis, Ribeirão Preto, SP, Brasil, August 17-20, 1996. We investigated the effects of losartan, an AT1-receptor blocker, and ramipril, a converting enzyme inhibitor, on the pressor response induced by angiotensin II (ANG II) and carbachol (a cholinergic receptor agonist). The injection of losartan (50 nmol/1 μl) into the LV blocked the pressor response induced by ANG II (12 ng/1 μl) and carbachol (2 nmol/1 μl).
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More From: Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
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