Background of hyperkinetic circulatory state in young spontaneously hypertensive rats.

Abstract

The present study explores the relationship between central hyperreactivity to alerting stimuli and the presence of a hyperkinetic circulatory state during “rest ” in very young spontaneously hypertensive rats (SHR). 6 week old SHR, ordinary normotensive Wistar rats (NCR) and normotensive Wistar rats of the Kyoto strain (WKR) were fitted with chronic catheters in the right carotid artery and jugular vein. The rats were habituated to the laboratory environment before the actual experiment, which included measurement of cardiac output (CO), mean arterial pressure (MAP) and heart rate (HR). CO was determined by a cardiogreen dye-dilution technique in microscale. Measurements were first performed when the rats were awake and at rest, thereafter when exposed to shortlasting “mental stress”, then during pentobarbitone anaesthesia, and finally during anaesthesia combined with pharmacological blockade of the neurogenic control of the heart. Thus, central haemodynamics could be followed over a wide range of neurogenic cardiac stimulation, from complete blockade over to intense physiological stimulation during mental stress. Young SHR with a 30% MAP elevation had a higher CO at rest than either of the controls, primarily because of increased HR. During “mental stress” the pattern of increased CO and HR in SHR was further accentuated. Elimination of mental excitatory stimuli by anaesthesia, and a subsequent cardiac neurogenic blockade, lowered CO and HR more in SHR than in the controls. Following these interventions CO was similar in all groups, but MAP remained elevated in SHR because of an increased total peripheral resistance (TPR). Further, for any given CO level both MAP and TPR were always higher in SHR than in either NCR or WKR, indicative that there are already structural vascular changes in 6 week old SHR. The results further suggest that the centrally mediated cardiovascular hyperreactivity to environmental stimuli also greatly influences basal haemodynamics in young SHR and are therefore of major importance in inducing this variant of primary hypertension.