Angiotensin II-mediated catecholamine release during the pressor response in rats

Abstract

Angiotensin II (ANG II)-mediated catecholamine release and its possible contribution to the pressor response was assessed in baroreceptor-denervated rats. Neonatal male Sprague-Dawley rats were injected with the sympatholytic drug, guanethidine monosulphate (50 mg/kg s.c., 6 days/week) for 40 days. Plasma catecholamine concentrations were measured using a 3H-radioenzymatic assay as follows: (a) before and 30 s after the injection of saline or ANG II (79.3 pmol/kg i.v.), at the peak of the pressor response, then 50 s and 80 s thereafter, in guanethidine-treated (GUAN) and saline-injected (SHAM) rats, and (b) before and after adrenalectomy (ADX), following the same time-sequence for ANG II as in (a). Peak pressor responses to graded doses of ANG II (6.6, 26.4, 53.0 and 79.3 pmol/kg i.v.) were measured in GUAN+ADX and ADX rats. Destruction of peripheral sympathetic nerves was confirmed by measurements of plasma noradrenaline (NA), adrenaline (AD) and dopamine (DA) concentrations and by changes in pressor responses and heart rates following i.v. doses of tyramine. ANG II induced significantly (P < 0.05) greater pressor responses in GUAN+ADX rats than in ADX rats, especially after the 53.0 and 79.3 pmol/kg doses. Plasma AD concentrations increased within seconds after the pressor response to ANG II in both GUAN and SHAM rats but there was no change in plasma NA or DA concentrations (P < 0.05). ANG-II-mediated AD release from the adrenal medulla may contribute to the overall pressor action of the peptide. The vasculature became more sensitive to ANG II at a time when NA and DA depletion occurred following sympathectomy and/or adrenalectomy. This heightened sensitivity to ANG II was not due to a decrease in circulating ANG II in sympathectomized rats because even though plasma renin activity fell from 6.54 +/- 0.52 to 3.77 +/- 0.26 ng ANG I/ml per h it remained within the normal range.

Dietary sodium chloride restriction enhances aortic wall lipid storage and raises plasma lipid concentration in LDL receptor knockout mice

“…Accordingly, an increase of the latter together with the plasma norepinephrine concentration has been reported in experimental normotensive animals and humans submitted to LSD. In addition, the higher concentration of plasma angiotensin II in LSD animals stimulates the release of norepinephrine from sympathetic nerve terminals, as well as of epinephrine from the adrenal medulla (28,29) that contribute to an insulin resistance state (30)(31)(32). This sympathetic overactivity elicits a reduction of the blood flow in peripheral tissues due to vasoconstriction, which includes the precapillary arteriolar sphincters in adipose tissue, and, simultaneously, enhances the adipose tissue lipolysis rate leading to an increase in the plasma NEFA concentration (30,31,33).…”

Evidence of angiotensin II involvement in prolactin secretion in response to hemorrhage in adrenodemedullated and guanethidine-treated rats

“…During stress, excited sympathetic nerves potentiate the activation of the RAS mediated by b-adrenergic receptors (42,50). Angiotensin II produced from the RAS subsequently facilitates the additional release of noradrenaline from sympathetic nerve endings (42) and of adrenaline from the adrenal medulla (51)(52)(53). This is also a positive feedback leading to a stronger excitation and secretion by the sympathetic-adrenal medulla system and a greater release of angiotensin II.…”

Sex-specific programming of hypertension in offspring of late-gestation diabetic rats

“…as bolus injection, with the volume of agent adjusted to 0.1 ml. The doses used for the various pharmacologic agents administered in vivo were chosen based upon review of the literature, and preliminary studies examining the range of responses to the agents 40–42 . Hemodynamic responses to increasing doses of phenylephrine, sodium nitroprusside, and angiotensin II are reported as a maximal percentile change from resting blood pressure and heart rate immediately prior to giving the drugs.…”