Pressor responses to intracisternal administration of hypertonic NaCl in conscious normotensive and spontaneously hypertensive rats.

We evaluated the mechanisms of pressor responses to hypertonic NaCl solution administered intracisternally (i.c.) to conscious normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). In conscious rats of both strains, increases in mean arterial pressure (MAP) and heart rate (HR) induced by i.c. NaCl appeared immediately after the injection and MAP returned rapidly to the basal levels. In the urethane-anesthetized animals, the increases in MAP and HR occurred gradually and persisted. The early phase of the pressor actions of i.c. NaCl was considered to be mostly abolished by blockade of the sympathetic nervous system (SNS), and to be partly diminished by the vascular receptor blockade of vasopressin (AVP), in the conscious animals. The following phase of pressor responses to i.c. NaCl was not suppressed by the blockade of ganglionic transmission, alpha-adrenergic receptor, AVP or angiotensin II (AII). However, bilateral adrenalectomy practically abolished the pressor action of both early and late phases, thereby suggesting that catecholamines (CA), released from the adrenal gland, may play a major role in this pressor response to i.c. NaCl. The pressor responses to i.c. NaCl in conscious or anesthetized animals were slightly but significantly greater in SHR than in WKY. It is concluded that an early phase of increase in MAP, as induced by hypertonic NaCl administered i.c. to conscious SHR and WKY, may be attributed mainly to the increased activity of the SNS and partly to the increased release of AVP. The major part of the pressor effect of i.c. NaCl, including the late phase, may result from an enhanced secretion of CA from the adrenal gland. The present study also shows that the pressor action of i.c. NaCl in rats may be altered when the animals are anesthetized with urethane.