The Nature of the β-Adrenoreceptor Controlling Plasma Renin Activity in Man

Johnson, Brian F. G.; Smith, I. K.; LaBrooy, Justin T.; Bye, Carole

doi:10.1042/cs051113s

Cited by 7 publications

(4 citation statements)

References 5 publications

(5 reference statements)

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“…( 1977) showed recently that renal renin release also depends on activation of a ,B2-adrenergic receptor. A. similar conclusion has been reached for man (Amery et al 1974;Johnson et al 1976). 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%.…”

Section: E~pgirinztv7tmentioning

confidence: 50%

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: 50%

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

Katovich¹,

Fregly²

1978

Can. J. Physiol. Pharmacol.

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“…Release of renin from the kidney by sympathetic nerve stimulation is blocked by propranolol (Davis and Freeman, 1976), but the /? adrenoceptor that mediates this release has been classified both as /?-l (Johnson et al, 1976) and /?-2 (Johns and Singer, 1974). The /?…”

Section: Discussionmentioning

confidence: 99%

Evidence for lack of innervation of beta-2 adrenoceptors in the blood vessels of the gracilis muscle of the dog.

Russell¹,

Moran²

1980

Circulation Research

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Cardiac /S-l adrenoceptors respond to sympathetic nerve stimulation (SNS), but it is not clear that SNS evokes fi-2 adrenoceptor-mediated vasodilation. Sensitivity of B adrenoceptors to catecholamines and to SNS was evaluated in dogs. Norepinephrine (NE) and epinephrine (E) were equipotent vasoconstrictors (femoral artery blood flow or gracilis autoperfusion pressure) before aadrenoceptor blockade with dibozane (DIB). After DIB, NE was 1/100 as potent a vasodilator as E, which was equipotent with isoproterenol (ISO). SNS evoked gracilis muscle vasoconstriction before DIB and vasodilation after. Dilation induced by SNS or acetylcholine (ACH) after DIB was blocked by atropine (AT), but that caused by NE was not. Dilation evoked by NE, E, or I after DIB and AT was blocked by propranolol (PROP). Vasoconstrictor responses to NE, E, or SNS in dogs without DIB were not augmented by PROP at a dose that blocked the dilator effect of ISO. NE and E were equipotent and both 1/10 as potent as ISO as positive inotropic and chronotropic agents. Cardiac responses to NE, E, ISO, and SNS were antagonized by PROP. Subclassification of adrenoceptors that subserve cardiac stimulation as fi-1 and that subserve vasodilation as fi-2 was substantiated. Cardiac fi-1 adrenoceptors responded to SNS and to circulating E and NE. Vascular fi-2 adrenoceptors responded to circulating E, to ISO, and to high doses of NE, but not to SNS. fi-2 Adrenoceptors in blood vessels appear not to be innervated and may function as hormone receptors sensitive primarily to E released from the adrenal medulla, rather than to NE released from adrenergic nerves.

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“…In normal man intravenous infusion of isoprenaline results in a dose-related rise in levels of plasma renin activity (Johnson, Smith, Labrooy & Bye, 1976a;Davies, Slater, Rudolph & Geddes, 1977;Harms, Gooren, Spoelstra, Hesse & Verschoor, 1978). In both tetraplegic patients and control subjects isoprenaline produced a twofold elevation in levels of plasma renin activity.…”

Section: Discussionmentioning

confidence: 97%

Renin and Aldosterone Release during Sympathetic Stimulation in Tetraplegia

et al. 1981

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1. The effect of endogenous sympathetic stimulation (induced by urinary bladder stimulation) and intravenous infusion of noradrenaline and isoprenaline on blood pressure, heart rate and levels of plasma renin activity and plasma aldosterone were studied in six tetraplegic patients. Data from infusion studies were compared with data from six normal subjects studied in an identical manner. 2. Bladder stimulation in the tetraplegic patients caused a marked rise in blood pressure and fall in heart rate, but no change in plasma renin activity or plasma aldosterone. 3. Noradrenaline infusion resulted in an enchanced pressor response in the tetraplegic patients when compared with the normal subjects. Heart rate fell in both groups. Plasma renin activity and plasma aldosterone did not change in either group. 4. Isoprenaline infusion caused a fall in both systolic and diastolic blood pressure in the tetraplegic patients, unlike the normal subjects in whom there was a rise in systolic and a fall in diastolic blood pressure. Heart rate and plasma renin activity rose in both groups. Plasma aldosterone did not change in either group. 5. We conclude that in tetraplegic patients neither endogenous sympathetic stimulation by bladder stimulation nor infusion of noradrenaline raises plasma renin activity. Isoprenaline increases plasma renin activity to the same extent as in normal subjects. Renin release mechanisms in tetraplegic patients therefore do not appear to be hypersensitive to catecholamines. Plasma aldosterone is not influenced by any of the stimuli.

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The Nature of the β-Adrenoreceptor Controlling Plasma Renin Activity in Man

Cited by 7 publications

References 5 publications

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

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

Evidence for lack of innervation of beta-2 adrenoceptors in the blood vessels of the gracilis muscle of the dog.

Renin and Aldosterone Release during Sympathetic Stimulation in Tetraplegia

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The Nature of the β-Adrenoreceptor Controlling Plasma Renin Activity in Man

Cited by 7 publications

References 5 publications

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

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

Evidence for lack of innervation of beta-2 adrenoceptors in the blood vessels of the gracilis muscle of the dog.

Renin and Aldosterone Release during Sympathetic Stimulation in Tetraplegia

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Product

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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