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PubMed2001

Do most antihypertensive agents have a sympatholytic action?

The sympathetic nervous system is a major modulator of cardiovascular functions. Over the past three decades, numerous studies, using various methodologies, have reported the existence of a variety of pre- and postsynaptic sympathetic dysfunctions in essential hypertension. Most of those abnormalities facilitate sympathetic neurotransmission, resulting in a chronic increase in the sympathetic tone and reactivity in an important proportion of hypertensive patients. The chronic sympathetic activation is also associated with major alterations in the balance between postsynaptic adrenergic receptors in cardiovascular tissues. Indeed, an attenuation of beta-adrenergic functions and a potentiation of alpha1-adrenergic functions have been demonstrated in human cardiovascular tissues, suggesting the development of a sympathetic postsynaptic alpha1 dominance during the development and evolution of hypertension. The chronic activation of the sympathetic system is deleterious and could contribute to the development of most cardiovascular complications associated with hypertension. One of the major aims of antihypertensive therapy should be to attenuate pre- or postsynaptic sympathetic tone. Most antihypertensive drugs have been found to improve either pre- or postsynaptic sympathetic functions in hypertensive patients. At the presynaptic level, the effects of antihypertensive drugs have been found to be more variable. At the postsynaptic level, all currently used antihypertensive drugs have been found to attenuate alpha1-adrenergic functions either by interfering directly with intracellular mechanisms underlying alpha1-adrenergic functions or indirectly by decreasing the release of norepinephrine from peripheral sympathetic nerves.

Antihypertensive Agents↗
PubMed1993

Role of the nucleus tractus solitarii and the rostral depressive area in the sympatholytic effect of 8-hydroxy-2-(di-n-propylamino)tetralin in the cat.

Bilateral microinjections of kainic acid (500 ng/site) into the nucleus tractus solitarii produced hypertension, tachycardia and sympatho-excitation in anesthetized cats. The cardiac-related component of renal sympathetic nerve activity was abolished as well as the sympatho-inhibitory effects that accompany the phenylephrine (5-10 micrograms/kg i.v.)-induced hypertension. About 60 min after kainic acid microinjections into the nucleus tractus solitarii, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) administered in cumulative doses (1-100 micrograms/kg i.v.) failed to alter mean blood pressure, heart rate or renal sympathetic nerve activity. In addition, bilateral microinjections of 8-OH-DPAT (2 nmol in 40 nl) into the nucleus tractus solitarii did not change mean blood pressure, heart rate or renal sympathetic nerve activity. Microinjections of kainic acid into the rostral vasodepressive area produced hypotension, bradycardia and renal sympatho-inhibition followed by persistent increases in blood pressure, heart rate and renal sympathetic nerve activity. These effects were also associated with an inhibition of the baroreceptor reflex elicited by phenylephrine and by the disappearance of the synchronism between the renal sympathetic bursts and cardiac rhythm. Subsequent i.v. 8-OH-DPAT (1-100 micrograms/kg) elicited decreases in mean blood pressure, heart rate and in renal sympathetic nerve activity. Central baroreceptor denervation by kainic acid lesions of the lateral tegmental field largely attenuated the hypotensive, bradycardiac and sympatho-inhibitory effects elicited by 8-OH-DPAT applied to the ventral surface of the rostral ventrolateral medulla.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1985

Sociosexual behaviors of female rats during and after chronic treatment with the sympatholytic agent guanethidine.

Ovariectomized female rats were chronically administered saline or guanethidine sulfate, a drug that blocks adrenergic neurons and, when chronically administered, results in peripheral sympathectomy. The females were periodically injected with estradiol benzoate and progesterone and tested for sexual behaviors before, during and after the six-week period of daily guanethidine or saline injections. Tests for copulatory behavior included tests for lordotic responsiveness to manual stimulation and tests of sociosexual behaviors displayed by the females in a complex testing environment. The complex environment permitted the test females to control their coital contacts with sexually active males and their interactions with sexually inactive males and ovariectomized female rats. Guanethidine treatment did not alter lordotic responsiveness to manual stimulation but did reduce the frequency of copulatory acts engaged in by the females in the complex environment. During the first test in the complex environment following the start of drug injections, the guanethidine-treated females, in comparison to saline-treated females, displayed a lower frequency of lordotic behavior during coital contacts. The changes in behavior produced by the sympathetic drug, guanethidine, implicate the autonomic nervous system in the regulation of copulatory pacing in the female rat.

Animals↗
PubMed1981

Phalloidin hepatotoxicity in rats in vivo. Effect of a sympatholytic agent: propranolol.

Phalloidin, one of the main toxins of Amanita phalloides, induced hepatotoxicity in female Wistar rats at 0.9 mg/kg dose i.p. Biliary secretion was selectively inhibited after 3h, but was restored after 24 h. Phalloidin also induced a cytolytic lesion, but not a fatty liver, as in alpha-amanitin intoxication. Propranolol pretreatment (30 min prior to phalloidin injection) did not afford protection against hepatotoxicity, but increased alkaline phosphatase, 5'-nucleotidase and aminotransferase activities.

Animals↗
PubMed1990

Dietary Ca2+ prevents NaCl-sensitive hypertension in spontaneously hypertensive rats by a sympatholytic mechanism.

The current study tested the hypothesis that dietary Ca2+ supplementation reverses the NaCl-sensitive component of hypertension and the associated neurochemical abnormalities in the NaCl-sensitive spontaneously hypertensive rat (SHR-S). Male SHR-S were begun on one of four diets at 8 weeks of age: control (0.75% NaCl/0.68% Ca2+); high NaCl (8.00% NaCl/0.68% Ca2+); high Ca2+ (0.75% NaCl/2.00% Ca2+); and high NaCl/high Ca2+ (8.00% NaCl/2.00% Ca2+). High NaCl SHR-S (X2 weeks) had higher mean arterial pressure (MAP) (161 +/- 4 mm Hg) than controls (149 +/- 3 mm Hg; P less than .05). Supplementation with Ca2+ prevented the rise in MAP in high NaCl rats, but did not alter MAP in controls. The 8% NaCl diet elevated plasma norepinephrine and reduced anterior hypothalamic (AHA) norepinephrine stores and turnover; concomitant Ca2+ supplementation restored both plasma norepinephrine and AHA norepinephrine turnover to normal. Clonidine was microinjected into the AHA of rats maintained on the four diets for 2 weeks to test the hypothesis that dietary Ca2+ supplementation prevents the previously observed NaCl-induced upregulation of alpha 2-adrenoceptors in AHA. Clonidine caused dose-dependent decreases in MAP that were greater in high NaCl rats than in controls. The Ca2+ supplementation prevented the exaggerated depressor response to clonidine in the high NaCl group, but not in the controls. The Ca2+ supplementation had no effect on pretreatment MAP or on MAP responses to clonidine in control NaCl-resistant SHR (SHR-R) or Wistar-Kyoto (WKY) rats. Thus, dietary Ca2+ supplementation prevents the NaCl-induced exacerbation of hypertension and augmented depressor response to clonidine in SHR-S by increasing noradrenergic input to AHA, thereby preventing the upregulation of AHA alpha 2-adrenoceptors.

Animals↗
PubMed1987

Sympatholytic effects of the intravenously injected alpha 1-adrenergic blocker, bunazosin, in anaesthetized rats.

Cardiovascular regulation during alpha 1-adrenergic blocker-induced vasodepression was investigated in urethane-anaesthetized rats. Intravenous (i.v.) injections of bunazosin, an alpha 1-blocker, elicited depressor responses which were accompanied by corresponding decreases in both heart rate and abdominal sympathetic discharge, dose-dependently. Those responses were not affected by the bilateral sino-aortic de-afferentation. Assuming that the site of action is in the central nervous system, bunazosin was injected intracerebroventricularly (i.c.v.). It produced hypotension accompanied by decreases in heart rate and abdominal sympathetic nerve activity. The magnitude of the responses was greater when bunazosin was injected i.c.v. than when injected i.v. Since these results indicated that the central alpha 1-adrenergic receptors mediate vasopressor responses, the effects of i.c.v. injections of an alpha 1-agonist, phenylephrine was explored. It elicited vasopressor responses accompanied by corresponding increases in heart rate and abdominal sympathetic nerve activity. Furthermore, i.c.v. pretreatment with bunazosin abolished the vasopressor responses to i.c.v. injections of phenylephrine. These results indicate that central alpha 1-adrenergic receptors mediate vasopressor responses and that i.v. injections of alpha 1-blockers affect the central alpha 1-receptors, to produce a decrease in sympathetic nerve activity. Consequently, alpha 1-adrenergic blockers decrease blood pressure not only by peripheral vasodilation but also by inhibition of the sympathetic outflow in rats.

Adrenergic alpha-Antagonists↗