Difference in vasopressin-induced contraction of basilar arteries from stroke-prone spontaneously-hypertensive rats (SP-SHR) and control Wistar-Kyoto rats (WKY).

Vasopressin (0.01-0.3 IU/ml) contracted isolated segments of rat basilar arteries from stroke-prone SHR (SP-SHR) and normotensive Wistar-Kyoto rats (WKY) unequally. Basilar arteries from SP-SHR were more responsive to vasopressin than were those from WKY when adrenergic nerve endings were present in both preparations. After destruction of adrenergic nerve endings by in vitro 6-hydroxydopamine treatment, the ED50 for vasopressin in both WKY and SP-SHR arteries decreased by a factor of three, indicating that the contractions caused by vasopressin were similarly modulated by prejunctional neurotransmitter release. However, only arteries from WKY showed prominent rhythmic relaxation-contraction cycles superimposed upon the vasopressin-induced tone. The tension cycles were 20-100 dyn in amplitude and occurred at 1-3 cycles/min. These tension oscillations of WKY were pronounced and obvious, sometimes amounting to as much tension as the underlying tonic contraction. Tension cycles could reflect a physiological contraction-relaxation phasing mechanism that fails to occur in basilar arteries of SP-SHR. The rhythmic activity was enhanced by K+-free solution and abolished by 30 mM K+ solution, suggesting that pacemaker changes in K+ conductance may underlie the WKY tension oscillations. It is suggested that the absence of rhythmic contractions in SP-SHR basilar arteries may be explained by greater activity of the electrogenic Na+-pump, which would tend to prevent the rhythmic oscillations in tension. These observations suggest that vasopressin has a differential action on basilar arteries of SP-SHR and WKY.