Dietary and pharmacological alterations in endogenous angiotensin II: effect on noradrenaline pressor responsiveness in the rat

Abstract

1 Rats were placed on either a low sodium intake (low sodium diet 0.025% dry weight, tap water for drinking) or a high sodium intake (normal sodium diet 0.45% dry weight, 0.9% saline for drinking) for 10 days. The pressor-response curve to angiotensin II in rats previously on a high sodium intake was shifted to the left of that found in rats previously on a low sodium intake. 2 Suppression of endogenous angiotensin II formation with captopril (0.3 mg kg-') or acute volume repletion (3% body wt per 30 min) resulted in a significant parallel shift of the pressor-response curve for angiotensin II to the left in the low salt group. In the high salt group captopril produced a similar but smaller parallel shift of the dose-response curve to the left. 3 Similar manipulation of endogenous angiotensin II concentrations with high and low salt intake plus captopril treatment or acute volume repletion, produced no alterations in the pressor response for noradrenaline. 4 The attenuated in vivo response to angiotensin II in the low salt intake group may be explained in part by the suppressed vascular sensitivity to angiotensin II in this group, as measured in the isolated perfused kidney of the rat. In kidneys from rats previously on a low sodium intake, an enhanced maximal vasoconstrictor response to noradrenaline was observed as compared to kidneys from high sodium intake rats. 5 These results indicate that, whereas alterations in endogenous angiotensin II concentrations within physiological limits affects the response to exogenous angiotensin, there is little if any effect on the pressor response to noradrenaline.

Modulation by Cytochrome P450-4A ω-Hydroxylase Enzymes of Adrenergic Vasoconstriction and Response to Reduced PO2 in Mesenteric Resistance Arteries of Dahl Salt-Sensitive Rats

“…Nonetheless, the effect of HS diet per se on vasoconstrictor or pressor responses in normotensive and hypertensive subjects is incompletely understood. For example, there are conflicting reports as to whether HS diet affects vascular responses to norepinephrine [2,16,18,37,38,42,53] or angiotensin II [16,34,53] in SS and salt‐insensitive experimental models. This is an important question, because any increase in the sensitivity to vasoconstrictor stimuli may aggravate the consequences of endothelial dysfunction and impaired vascular relaxation, contributing to an elevation of total peripheral resistance and an increase in arterial blood pressure.…”