The role of angiotensin in thirst

Severs, Walter B.; Summy-Long, Joan Y.

doi:10.1016/0024-3205(75)90172-1

Cited by 65 publications

(9 citation statements)

References 69 publications

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“…Thc weight sf current evidence suggests that isoproterenol-induczd thirst is mediated via the renin-angioteansin system (Bryant aiad FaIk 1973;Fitzsianons and Simons 1969;Fitzsirno~ms 1969Fitzsirno~ms , 1972Fitzsirno~ms , 1975Gutman et a%. 1971 ;Severs and Summy-Long 1975). Hence, the possibility exists that the p2-adrenergic receptors associated with isoprotereno1-induced thirst may be the same receptors associated with renin release.…”

Section: E~pgirinztv7tmentioning

confidence: 96%

Mediation of isoproterenol-induced thirst in rats by β₂-adrenergic receptors

Katovich¹,

Fregly²

1978

Can. J. Physiol. Pharmacol.

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Isoproterenol-induced thirst in rats has been attributed to the activation of beta-adrenergic receptors. Since these receptors can be further differentiated pharmacologically into beta1 and beta2 types, experiments were performed using several beta-adrenergic agonists and antagonists to determine the receptor type initiating the isoproterenol-induced thirst. The beta1- and beta2-adrenergic antagonist, d,l-propranolol (1 mg/kg, ip), blocked the increase in water intake usually accompanying acute subcutaneous administration of isoproterenol (25 microgram/kg) to female rats. Since l-propranolol is known to stabilize membranes and to possess anesthetic-like properties, d-propranolol was also used. This isomer has little beta-adrenergic-blocking activity but possesses anesthetic-like activity. Administration of d-propranolol (1 mg/kg, ip) failed to affect the drinking response to acute administration of isoproterenol (25 microgram/kg). Practolol (125 mg/kg), a beta1-adrenergic antagonist with little anesthetic properties, also had no effect on water intake of isoproterenol-treated rats. Butoxamine, a selective beta2-adrenergic antagonist, attenuated the drinking response to isoproterenol. Salbutamol (150 microgram/kg), a beta2-adrenergic agonist, mimicked the effect of isoproterenol on water intake. These results are consistent with the suggestion that beta2-adrenergic receptors mediate the isoproterenol-induced thirst in rats.

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Section: E~pgirinztv7tmentioning

confidence: 96%

Mediation of isoproterenol-induced thirst in rats by β₂-adrenergic receptors

Katovich¹,

Fregly²

1978

Can. J. Physiol. Pharmacol.

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“…This was originally demonstrated when A-I1 was given intravenously to rats (1) and since has been demonstrated in a large number of species ( s e e reviews (2)(3)(4)). It is well documented that the administration of the octapeptide, angiotensin I1 (A-11), elicits drinking by animals.…”

mentioning

confidence: 93%

Intraventricular Angiotensin Elicits Drinking in the Baboon

Ec¹,

Ld²,

Ml³

et al. 1980

Experimental Biology and Medicine

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“…Fortunately, this has, to a large extent, been done by others. Areas that have been reviewed recently include the fo llowing: regulation of renin secretion (44,230); converting enzyme (56,198) ; angiotensin receptors (51) ; the role of the renin-angiotensin sys tem in the control of aldosterone secretion (43); actions of angiotensin II on the central nervous system (187,188); the "brain renin-angiotensin system" (70,165) ; actions of "angiotensin III" (60); antagonists of angio tensin (211); interactions between prostaglandins and the renin-angiotensin system (153).…”

Section: Introduction -:-1196mentioning

confidence: 99%

The Renin-Angiotensin System

Reid¹,

Morris²,

Ganong³

1978

Annu. Rev. Physiol.

523

176

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Since the discovery of renin 80 years ago, there have been remarkable advances in our understanding of the renin-angiotensin system. The system as it is known today is summarized in Figure 1. Angiotensin III, the active component of the system, has several important physiological actions. The fi rst of these to be identifi ed was its pressor action, and for many years it was felt that the sole function of the renin-angiotensin system was regula tion of blood pressure. A new dimension was added in 1960 with the discovery that angiotensin II stimulates the secretion of aldosterone and is therefore in a position to exert important effects on salt and water balance. Several additional actions of angiotensin II were then discovered. It was fo und that the peptide can increase the secretion of catecholamines from the adrenal and facilitate adrenergic transmission. It also acts directly on the brain to increase blood pressure via sympathetic and parasympathetic path ways, to produce thirst, and to stimulate the secretion of vasopressin and ACTH. Through these actions, the renin-angiotensin system plays an im portant role in the regulation of blood pressure and of the volume and composition of the extracellular fl uid.Major advances have also been made in our understanding of other aspects of the renin-angiotensin system. It has become clear that the hep tapeptide metabolite of angiotensin II, [des-Aspl] angiotensin II ("angioIThe IUPAC-IUB Commission on Biochemical Nomenclature Recommenda tions (J. Dial Chem.2S0:321S) has suggested that the peptide hormones referred to in this review-angiotensin I, angiotensin II, ACTH, and growth hormone-be termed proangiotensin, angiotensin, corticotropin, and somatotropin, respectively.

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The role of angiotensin in thirst

Cited by 65 publications

References 69 publications

Mediation of isoproterenol-induced thirst in rats by β₂-adrenergic receptors

Mediation of isoproterenol-induced thirst in rats by β₂-adrenergic receptors

Intraventricular Angiotensin Elicits Drinking in the Baboon

The Renin-Angiotensin System

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The role of angiotensin in thirst

Cited by 65 publications

References 69 publications

Mediation of isoproterenol-induced thirst in rats by β2-adrenergic receptors

Mediation of isoproterenol-induced thirst in rats by β2-adrenergic receptors

Intraventricular Angiotensin Elicits Drinking in the Baboon

The Renin-Angiotensin System

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Mediation of isoproterenol-induced thirst in rats by β₂-adrenergic receptors

Mediation of isoproterenol-induced thirst in rats by β₂-adrenergic receptors