Abstract
Cardiovascular sensitivity to anesthetics has been linked to the renin-angiotensin system (RAS), and it is thought to be related to the differences in cardiovascular collapse observed between SS and BN rats. In a previous study we found that congenics carrying the BN renin allele (renin+) in the SS background had the same cardiovascular sensitivity and low BK channel activity as BN rats. On the other hand, congenics carrying the SS renin allele (renin-) displayed high BK activity and behaved like SS rats, suggesting that RSA could be involved in differential responses. To test this hypothesis, the inhibition of BK channel by angiotensin II (AngII, 100 nM) was evaluated in four strains. Activity of BK was monitored from isolated mesenteric arterial smooth muscle cells of SS and BN rats, and renin+ and renin- congenic rats in the cell-attached mode at +80 mV Em and in symmetrical 150 mM K+. Blockade by paxilline (1 μM) confirmed identity of BK channel. Similar to findings from our previous study, in the cell-attached mode the probability of BK channel opening (Po) was different between SS (high Po) and BN (lower Po). The BK activity of renin2- resembled that of SS, whereas BK activity of renin+ matched BN. AngII had a greater inhibitory effect on channel Po in BN (−55+7%) and renin+ (−94+2%) strains than in SS (−9+6%) and renin- (−7+2%) strains. Impaired renin expression and impaired RAS are associated with lower sensitivity of BK to inhibition by AngII in SS than in BN rats. The fact that renin+ and renin- strains follow a similar pattern appears to support this conclusion.
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