Complete dissociation of DOCA-salt hypertension and red cell ion transport alterations.
Our previous study revealed major ion transport alterations that resulted in a pronounced elevation of red cell Na+ content in DOCA-salt treated homozygous vasopressin-deficient (DI) Brattleboro rats in which only a moderate increase of systolic blood pressure occurred. In contrast, no changes of red cell Na+ content were observed in heterozygous vasopressin-secreting (non-DI) Brattleboro rats with a severe DOCA-salt hypertension. Using a chronic supplementation of DI rats with an antidiuretic agonist dDAVP (1-desamino-8-D-arginine vasopressin) we did not demonstrate any significant changes of red cell ion transport in dDAVP-treated DI rats with a fully developed DOCA-salt hypertension. The absence of ion transport alterations seems to be mainly due to dDAVP-induced correction of altered K+ metabolism seen in DOCA-salt treated DI animals. It can be concluded that DOCA-salt hypertension can develop even without red cell ion transport alterations which are usually caused by cell K+ depletion.
Bin Talib
H K
HK
Institute of Physiology, Czechoslovak Academy of Sciences, Prague.
Kunes
J
J
Zicha
J
J
D000818:Animals; D001794:Blood Pressure; D001835:Body Weight; D003894:Deamino Arginine Vasopressin / Q000008:administration & dosage; D003900:Desoxycorticosterone; D004912:Erythrocytes / Q000378:metabolism*; D005260:Female; D006978:Hypertension, Renovascular / Q000378:metabolism*; D017136:Ion Transport; D009994:Osmolar Concentration; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D011910:Rats, Brattleboro; D012964:Sodium / Q000378:metabolism*; D014667:Vasopressins / Q000172:deficiency
D014667:Vasopressins; D003900:Desoxycorticosterone; D012964:Sodium; D003894:Deamino Arginine Vasopressin; D011188:Potassium