The cardiopulmonary reflexes of spontaneously hypertensive rats are normalized after regression of left ventricular hypertrophy and hypertension

Cardiopulmonary reflexes are activated via changes in cardiac filling press ure (volume-sensitive reflex) and chemical stimulation (chemosensitive refl ex). The sensitivity of the cardiopulmonary reflexes to these stimuli is im paired in the spontaneously hypertensive rat (SHR) and other models of hype rtension and is thought to be associated with cardiac hypertrophy. The pres ent study investigated whether the sensitivity of the cardiopulmonary refle xes in SHR is restored when cardiac hypertrophy and hypertension are reduce d by enalapril treatment. Untreated SHR and WKY rats were fed a normal diet . Another groups of rats were treated with enalapril (10 mg kg(-1) day(-1), mixed in the diet; SHRE or WKYE) for one month. After treatment, the volum e-sensitive reflex was evaluated in each group by determining the decrease in magnitude of the efferent renal sympathetic nerve activity (RSNA) produc ed by acute isotonic saline volume expansion. Chemoreflex sensitivity was e valuated by examining the bradycardia response elicited by phenyldiguanide administration. Cardiac hypertrophy was determined from the left ventricula r/body weight (LV/ BW) ratio. Volume expansion produced an attenuated renal sympathoinhibitory response in SHR as compared to WKY rats. As compared to the levels observed in normotensive WKY rats, however, enalapriI treatment restored the volume expansion-induced decrease in RSNA in SHRE. SHR with e stablished hypertension had a higher LV/BW ratio (45%) as compared to normo tensive WKY rats. With enalapril treatment, the LV/BW ratio was reduced to 19% in SHRE. Finally, the reflex-induced bradycardia response produced by p henyldiguanide was significantly attenuated in SHR compared to WKY rats, Un like the effects on the volume reflex, the sensitivity of the cardiac chemo sensitive reflex to phenyldiguanide was not restored by enalapril treatment in SHRE. Taken together, these results indicate that the impairment of the volume-sensitive, but not the chemosensitive, reflex can be restored by tr eatment of SHR with enalapril. It is possible that by augmenting the gain o f the volume-sensitive reflex control of RSNA, enalapril contributed to the reversal of cardiac hypertrophy and normalization of arterial blood pressu re in SHR.