Abnormal baroreflex control of heart rate in prehypertensive and hypertensive Dahl genetically salt-sensitive rats.
This study tested the hypothesis that in the Dahl model of genetic hypertension abnormal baroreflex function may precede and contribute to the development of hypertension. Sensitivity of baroreflex control of heart rate was assessed in conscious sensitive (S) and resistant (R) Dahl rats fed a high or low salt diet. Sensitivity of baroreflex control of heart rate was lower in S rats fed low salt although arterial pressure was not different from that of R rats. Hypertensive S rats showed resetting of baroreflexes to the higher pressure level without any further change in sensitivity. Pressor responses to phenylephrine were augmented in both prehypertensive and hypertensive S rats compared to R rats. Ganglionic blockade abolished this difference. In hypertensive S rats, ganglionic blockade decreased arterial pressure to levels not different than similarly treated R rats, indicating that neurogenic mechanisms contribute importantly to the early stages of hypertension in the Dahl model. These studies have identified impaired baroreflex function in prehypertensive and hypertensive Dahl S rats. This defect augments responses to pressor stimuli and may contribute to the development of salt-induced hypertension in the Dahl strain.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D005260:Female; D005730:Ganglionic Blockers / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology*; D005996:Nitroglycerin / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011311:Pressoreceptors / Q000503:physiopathology*; D051381:Rats; D012018:Reflex / Q000187:drug effects; D012965:Sodium Chloride / Q000494:pharmacology*
D005730:Ganglionic Blockers; D010656:Phenylephrine; D012965:Sodium Chloride; D005996:Nitroglycerin