Abstract
We studied the effect of guanilate cyclase signaling pathway on the diuretic and natriuretic renal functions in intact and hydrated WAG rats and also in vasopressin-deficient Brattleboro rats. We show that the direction of the changes in natriuretic function under conditions of guanilate cyclase signaling pathway activation is dependent on the blood vasopressin (Vp) level. In WAG rats with normal blood Vp level, the guanilate cyclase signaling cascade activation by NO synthesis activation by the exogenous donor sodium nitroprusside (SNP), as well as after the elimination of cGMP degradation by sildenafil administration, was accompanied by an antidiuretic response without any significant changes of hydruretic function. In contrast, in Brattleboro rats and hydrated WAG rats under SNP treatment, the the natriuretic reaction was observed. The cildenafil citrate administration in vasopressin-deficient Brattleboro rats was followed by the natriuresis, as well as the antiduiretic reaction, while in hydrated WAG rats the natriuretic reaction without any significant changes of natriuretic renal functions was observed. The possible mechanisms underlying the cAMP and cGMP signaling systems interaction that mediates the effects of the vasopressin and NO on the water and sodium transport are discussed.
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