Sympathetic activation in rats with L-NAME-induced hypertension

Abstract

We evaluated the hemodynamic pattern and the contribution of the sympathetic nervous system in conscious and anesthetized (1.4 g/kg urethane, iv) Wistar rats with L-NAME-induced hypertension (20 mg/ kg daily). The basal hemodynamic profile was similar for hypertensive animals, conscious (N = 12) or anesthetized (N = 12) treated with L-NAME for 2 or 7 days: increase of total peripheral resistance associated with a decrease of cardiac output (CO) compared to normotensive animals, conscious (N = 14) or anesthetized (N = 14). Sympathetic blockade with hexamethonium essentially caused a decrease in total peripheral resistance in hypertensive animals (conscious, 2 days: from (means ± SEM) 2.47 ± 0.08 to 2.14 ± 0.07; conscious, 7 days: from 2.85 ± 0.13 to 2.07 ± 0.33; anesthetized, 2 days: from 3.00 ± 0.09 to 1.83 ± 0.25 and anesthetized, 7 days: from 3.56 ± 0.11 to 1.53 ± 0.10 mmHg mL -1 min -1 ) with no change in CO in either group. However, in the normotensive group a fall in CO (conscious: from 125 ± 4.5 to 96 ± 4; anesthetized: from 118 ± 1.5 to 104 ± 5.5 mL/min) was observed. The responses after hexamethonium were more prominent in the hypertensive anesthetized group. However, no difference was observed between conscious and anesthetized normotensive rats in response to sympathetic blockade. The present study shows that the vasoconstriction in response to L-NAME was mediated by the sympathetic drive. The sympathetic tone plays an important role in the initiation and maintenance of hypertension.

Hypotensive effect of the water extract of the leaves of Pseuderanthemum palatiferum

“…The sympathetic tone plays an important role in the initiation and maintenance of hypertension. The hypertension induced by an NO blockade is associated with an increase in total peripheral resistance [12]. A similar response is found in humans [18].…”

Animal models for the study of arterial hypertension

“…As for the cardiac output, some evidence seems to indicate a reduction even during chronic inhibition of NO synthase. A likely sympatho-excitatory action of central origin has also been proposed by Biancardi et al (2007), who showed that vasoconstriction in response to L-NAME by the sympathetic tone plays an important role in the initiation and maintenance of hypertension.…”

Enantioselective pharmacokinetics and cardiovascular effects of nebivolol in L-NAME hypertensive rats

“…Nevertheless, it is well known that the hypertensive state in chronically treated L-NAME hypertensive animals is not only induced by the abolition of the NO system but also by overactivity of the renin-angiotensin system and the sympathetic nervous system. [25][26][27][28] Therefore, the increased hypotensive response to nebivolol in L-NAME hypertensive rats could be explained by its ability to reduce reninangiotensin and sympathetic overactivity. Previous studies have demonstrated that treatment with nebivolol reduces plasma renin and angiotensin II levels in spontaneously hypertensive rats.…”