Abstract
Comparison of norepinephrine (NE) sensitivity in caudal arterial muscle of rats with three forms of hypertension showed that there was no increase in either DOCA-salt or Dahl genetic hypertension, in contrast to the increased NE sensitivity found in spontaneously hypertensive rats (SHR). In hypertension induced by deoxycorticosterone acetate (DOCA)-salt treatment, as in Dahl genetic hypertension, there was also no difference in membrane potential (Em) between hypertensive and normotensive rats. By comparison to the SHR membrane alterations reported previously, any increased NE sensitivity might have been associated with altered Em electrogenesis which is triggered by a trophic factor of the sympathetic nervous system. SHR have a lower intracellular K+ free ion concentration and thus a smaller contribution of the ion gradient generated voltage which appears to be compensated for at rest by more active electrogenic ion transport. While SHR show greater depolarization and contraction than Wistar-Kyoto (WKY) rats in response to midrange NE concentrations, DOCA-salt and Dahl hypertensive rat caudal arterial muscle showed neither NE hypersensitivity nor any evidence of altered Em mechanisms. Ion transport in isolated peripheral arteries In DOCA-salt hypertension may only secondarily be altered in response to primary changes in humoral factors and altered neural control mechanisms.