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1 Research Center, Hopital Ste-Justine, Montreal, Quebec, Canada; Department of Obstetrics & Gynecology and Pharmacology, Universite de Montreal, Montreal, Quebec, Canada
* To whom correspondence should be addressed. E-mail: stlouisj{at}justine.umontreal.ca.
Gestation is associated with decreased blood pressure and resistance to the effects of vasoconstrictor agents. It has been reported recently that pregnant rats, on increased sodium intake, present physiological changes that resemble those observed in preeclampsia. We investigated the effects of sodium supplementation on reactivity and on potassium and calcium channel activity in blood vessels during gestation. Sodium supplements, 0.9% or 1.8% NaCl as drinking water, were given to non-pregnant and pregnant rats for 7 days (last week of gestation). Reactivity to phenylephrine (PhE), KCl, vasopressin (AVP) and tetraethylammonium (TEA) was measured in aortic rings under modulation of potassium and calcium channels. TEA, a nonselective K+ channel inhibitor, induced concentration-dependent responses in aortic rings from non-pregnant, but not in those from pregnant rats. The response to TEA was restored in rings from pregnant rats after pre-incubation with 10 mmol/L KCl. Sodium supplementation did not affect the response to TEA in the aortae of pregnant animals. After sodium supplementation, maximum responses to PhE and AVP were decreased and increased in aortic rings from nonpregnant and pregnant rats, respectively. Cromakalim (a KATP activator) -induced inhibition of the responses to the 3 vasoconstrictors was more striking in aorta from non pregnant than pregnant rats on regular diet, whereas it produced similar inhibition in tissues from both groups of animals on 0.9% and 1.8% NaCl. NS-1619 (a KCa activator) elicited heightened effects in the aorta of pregnant animal receiving 0.9% NaCl supplementation. Nifedipine (a Ca2+ channels blocker) caused greater inhibition of the contractile responses in tissues from non-pregnant rats on regular diet, and its action was increased in pregnant rats on sodium supplemented-diets. These data demonstrate that augmented sodium intake during gestation in the rat is linked with the reversal of gestational-associated resistance to vasopressors and indicate that this is an experimental model showing some features of gestational hypertension.
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