Mechanisms of pressor responses to intracisternal administration of hypertonic NaCl in conscious, unrestrained normotensive and spontaneously hypertensive rats.

We evaluated the mechanisms of pressor responses to hypertonic NaCl administered intracisternally (IC) to conscious normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Both mean arterial pressure (MAP) and heart rate (HR) increased immediately after IC NaCl (1.5mol/l, 60 microliters/kg), but MAP returned rapidly to the basal level. Pressor and tachycardic actions at the early phase were mostly abolished by either hexamethonium or phentolamine with the blockade of sympathetic nervous system (SNS), and slightly diminished by the V1-vasopressin blocker. In contrast, at the following phase pressor responses were not suppressed by combined or solitary blockade of SNS, vasopressin and angiotensin II (AII). The pressor effects of IC NaCl were slightly greater in SHR than in WKY. It is concluded that the early-phase increases in MAP by hypertonic NaCl administered IC to conscious SHR and WKY may be attributed mainly to the increased activity of SNS and partly to the increased release of AVP, although the late- phase pressor responses may result from some pressor factor(s), unrelated to SNS, AVP and AII.