Hormone Effects Upon Cyclic Nucleotide Excretion in Man

Immunohistochemical localization of 3′:5′-cyclic AMP and 3′:5′-cyclic GMP in rat renal cortex: Effect of parathyroid hormone

“…Because cGMP formation can be stimulated by calcium (17, 31; 34), conceivably the increase in calcium access (either from an intracellular depot or from, tubular fluid) to guanylate cyclase, evoked by cAMP, may result in the increase in cGMP formation concomitant with or consequent to the PTH-induced increase in cAMP. This model finds indirect support in the observations that nephrogenous urinary cGMP increases at the same time (13) or follows the increase in cAMP in response to exogenous or endogenous PTH (11)(12)(13)(14). Supporting this idea is the observation that, in slices from PTH-perfused kidneys, in which cAMP was elevated, cGMP fluorescence may be stimulated in situ by exposure to calcium (Fig.…”

“…PTH neither increases total tissue cGMP in renal cortical slices in vitro (8) nor stimulates cGMP formation in either homogenates from renal cortex (9) or preparations of glomeruli or tubules (10). On the other hand, in several studies, an increase in urinary cGMP was observed after PTH administration or after elevation of endogenous PTH (11)(12)(13)(14). It was not established in these studies whether increases in urinary cGMP excretion were due solely to a direct effect of PTH on intrarenal cGMP formation or were secondary to glomerular filtration of cGMP and active uptake of the nucleotide into…”

Prolonged antidiuresis by 1-desamino-8-D-arginine vasopressin (DDAVP): Correlation to its plasma levels and nephrogenous cyclic AMP production.

“…An intramuscular injection of synthetic lysine vasopressin at a dose of 0.1 pressor units/kg was also effective in raising the urinary cyclic AMP levels (Takahashi et al, 1966). Similar maneuvers, however, failed to result in an increase in cyclic AMP excretion in other studies (Williams et al, 1972 ;. Various or even conflicting results were obtained also in rats (Bulten and Jard, 1972 ;Chase and Aurbach, 1967).…”

“…The mean base-line nephrogenous cyclic AMP in patients was lower than in control subjects but the difference was not significant. This may be explained by the fact that several factors except vasopressin, a major one of which is parathyroid hormone , are involved in the regulation of urinary cyclic AMP excretion and that vasopressin-induced elevation of nephrogenous cyclic AMP is modest compared with that induced by parathyroid hormone (Williams et al, 1972 ;Bulten and Jard, 1972 ;Chase and Aurbach, 1967 ;Broadus et al, 1977) In any event, a small portion of nephrogenous cyclic AMP which was not suppressed by calcium infusion in normal subjects (Broadus et al, 1978) might be explained by vasopressin-dependent nephrogenous cyclic AMP.…”

The Effect of Pituitary-Adrenal Manipulations Upon Urinary Cyclic Amp Excretion in Man

“…In vivo studies in the rat (Peytremann et al 1973) and the sheep (Espiner et al 1974) have shown that the administration of pharmacologie amounts of ACTH significantly increase both ') Cyclic 3',5'-adenosine monophosphate tissue and plasma levels of cyclic AMP followed by maximal increases in plasma corticosteroids. On the other hand, in limited in vivo studies in man, Williams et al (1972) found no change in urinary cyclic AMP excretion with ACTH or cortisone administration. The present studies were undertaken in an effort to determine whether acute changes in pituitary-adrenal activity in man are associated with alteration in urinary cyclic AMP excretion.…”