Title : GABAergic excitation of vasopressin neurons: possible mechanism underlying sodium-dependent hypertension.

Pub. Date : 2013 Dec 6

PMID : 24103391






5 Functional Relationships(s)
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1 RATIONALE: Increased arginine-vasopressin (AVP) secretion is a key physiological response to hyperosmotic stress and may be part of the mechanism by which high-salt diets induce or exacerbate hypertension. Salts arginine vasopressin Rattus norvegicus
2 RATIONALE: Increased arginine-vasopressin (AVP) secretion is a key physiological response to hyperosmotic stress and may be part of the mechanism by which high-salt diets induce or exacerbate hypertension. Salts arginine vasopressin Rattus norvegicus
3 OBJECTIVE: Using deoxycorticosterone acetate-salt hypertension model rats, we sought to test the hypothesis that changes in GABA(A) receptor-mediated inhibition in AVP-secreting magnocellular neurons contribute to the generation of Na(+)-dependent hypertension. Salts arginine vasopressin Rattus norvegicus
4 The depolarizing GABA equilibrium potential shift in AVP-secreting neurons occurred progressively over weeks of deoxycorticosterone acetate-salt treatment along with gradual increases in plasma AVP and blood pressure. Salts arginine vasopressin Rattus norvegicus
5 Intracerebroventricular bumetanide administration during deoxycorticosterone acetate-salt treatment hindered the development of hypertension and rise in plasma AVP level. Salts arginine vasopressin Rattus norvegicus