Effect of adrenergic agents on toad bladder response to ADH, 3',5'-AMP, and theophylline

Handler, Jerome S.; Bensinger, Richard E.; Orloff, Jack

doi:10.1152/ajplegacy.1968.215.5.1024

Cited by 101 publications

(37 citation statements)

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“…Mongrel dogs, weighing [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25] kg, were anesthetized with Nembutal (Abbott Laboratories, North Chicago, Ill.), and the kidneys were removed rapidly and kept in ice-cold KrebsRinger bicarbonate buffer during the following procedures. The cortex, the red outer medulla, and the white inner medulla were studied separately.…”

Section: Methodsmentioning

confidence: 99%

“…Additionally, it has been shown that beta adrenergic stimuli induce an antidiuretic effect by unknown mechanisms (7)(8)(9), and that alpha-adrenergic stimuli cause a diuresis by inhibiting the effect of vasopressin to increase membrane permeability (8)(9)(10). In support of this latter concept Handler, Bensinger, and Orloff (11) demonstrated that alpha adrenergic agents inhibit the hydro-osmotic effect of vasopressin, but not of exogenous cyclic AMP. On the basis of these observations, they proposed that alpha adrenergic activity inhibits the effect of vasopressin to stimulate cyclic AMP generation.…”

Section: Introductionmentioning

confidence: 95%

“…I------strated to have a diuretic effect in mammalian kidneys (8)(9)(10), and to decrease water permeability in the isolated toad bladder (11). Handler, Bensinger, and Orloff, and Liberman, Klein, and Kleeman (10,11) proposed that this diuretic effect of alpha adrenergic agents is mediated by decreasing the ability of vasopressin to stimulate cyclic AMP generation.…”

mentioning

confidence: 99%

“…Handler, Bensinger, and Orloff, and Liberman, Klein, and Kleeman (10,11) proposed that this diuretic effect of alpha adrenergic agents is mediated by decreasing the ability of vasopressin to stimulate cyclic AMP generation. The observation that alpha adrenergic stimulus inhibits the effect of vasopressin to increase cyclic AMP concentration is consistent with that hypothesis.…”

mentioning

confidence: 99%

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Effects of Catecholamines and their Interaction with Other Hormones on Cyclic 3′,5′-Adenosine Monophosphate of the Kidney

Beck¹,

Reed²,

Murdaugh³

et al. 1972

J. Clin. Invest.

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A B S T R A C T Catecholamines have several physiological effects on the kidney. These include: (a) stimulation of renin synthesis in the cortex; (b) antidiuresis by beta adrenergic agents; and (c) diuresis by alpha adrenergic stimulation. The role of cyclic 3',5'-adenosine monophosphate (cyclic AMP) in the renal actions of catecholamines was evaluated by measuring the effects of several adrenergic agents on cyclic AMP concentration in the dog kidney.Beta adrenergic activity increased cyclic AMP concentration in the renal cortex, a finding consistent with the hypothesis that beta-adrenergic stimulation augments renin synthesis by increasing cyclic AMP generation.Beta adrenergic stimulation, like vasopressin, increased cyclic AMP concentration in the renal medulla. This suggests that beta adrenergic stimulation causes antidiuresis by augmenting cyclic AMP generation in the renal medulla.Alpha adrenergic activity inhibited the effect of vasopressin to stimulate cyclic AMP generation. These results support the hypothesis that the diuretic effect of alpha adrenergic stimulation is mediated by inhibition of the effect of vasopressin to increase cyclic AMP generation.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Effects of Catecholamines and their Interaction with Other Hormones on Cyclic 3′,5′-Adenosine Monophosphate of the Kidney

Beck¹,

Reed²,

Murdaugh³

et al. 1972

J. Clin. Invest.

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“…In vitro beta adrenergic drugs increase and alpha adrenergic drugs decrease renal cyclic AMP generation but in the toad bladder an effect of catecholamines on water movement can only be demonstrated in the presence of vasopressin (29) (30). Similarly the effect of PGE in both toad bladder and collecting duct may be due to inhibition of ADH activation of adenyl cyclase since PGE causes no inhibition of water movement induced by cyclic AMP (31).…”

Section: Resultsmentioning

confidence: 99%

Studies of the mechanism of contralateral polyuria after renal artery stenosis.

Galvez¹,

Roberts²,

Mishkind³

et al. 1977

J. Clin. Invest.

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A B S T R A C T Acute renal artery stenosis in hydropenic dogs caused a contralateral increase in urine volume and free water clearance without change in glomerular filtration, renal blood flow, or osmolar clearance. The increase in urine volume was not dependent on the development of hypertension since it occurred in animals pretreated with trimethaphan but was dependent upon angiotensin since it was prevented with angiotensin blockade with Saralasin. The effect was not caused by angiotensin inhibiting antidiuretic hormone release since the polyuria occurred in hypophysectomized animals receiving a constant infusion of 10 uU/kg per min of aqueous Pitressin. Since the rise in urine volume was associated with an increase in renal vein prostaglandin E concentration and was prevented by pretreatment with indomethacin (5 mg/kg) the results suggest that the rise in plasma angiotensin after renal artery stenosis causes an increase in contralateral prostaglandin E synthesis with resultant antagonism to antidiuretic hormone at the collecting tubule.

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Untersuchungen zur Wirkungsweise der Hormone (Nobel‐Vortrag)

Sutherland

1972

Angewandte Chemie

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Effect of adrenergic agents on toad bladder response to ADH, 3',5'-AMP, and theophylline

Cited by 101 publications

References 0 publications

Effects of Catecholamines and their Interaction with Other Hormones on Cyclic 3′,5′-Adenosine Monophosphate of the Kidney

Effects of Catecholamines and their Interaction with Other Hormones on Cyclic 3′,5′-Adenosine Monophosphate of the Kidney

Studies of the mechanism of contralateral polyuria after renal artery stenosis.

Untersuchungen zur Wirkungsweise der Hormone (Nobel‐Vortrag)

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