SPONTANEOUSLY HYPERTENSIVE RAT Y-CHROMOSOME INCREASES INDEXES OF SYMPATHETIC NERVOUS-SYSTEM ACTIVITY

Previous studies from our laboratory have demonstrated that the Y chro mosome from the spontaneously hypertensive rat (SHR) is responsible fo r a significant portion of the elevated blood pressure and also produc es an earlier pubertal rise in plasma testosterone. We performed the f ollowing studies to determine whether the SHR Y chromosome raises bloo d pressure by sympathetic nervous system responses as measured by adre nal chromogranin A and plasma and tissue catecholamines. Male SHR from The University of Akron colony were studied from 5 to 20 weeks of age . Blood pressure was measured by tail-cuff, tail artery cannulation, a nd aortic telemetry (Data Sciences); acute (air stress) and chronic (t erritorial colony) social stressors were compared; blood was collected for determination of plasma catecholamines; and adrenal glands were a nalyzed at 15 weeks for catecholamines. Rats with the SHR Y chromosome had higher blood pressure and plasma norepinephrine than those with t he normotensive Wistar-Kyoto (WKY) Y chromosome. However, the SHR Y ch romosome did not significantly change responsive ness to acute or chro nic stressors. Phentolamine and clonidine prevented the stress respons es. Adrenal chromogranin A levels were elevated 37% and 40% and adrena l norepinephrine content 29% and 100% at 4 and 10 weeks of age, respec tively, in rats with an SHR Y chromosome compared with WKY. Chemical s ympathectomy normalized blood pressure in all strains and significantl y reduced norepinephrine (36% to 42%) in all strains except in WKY, wh ich already had a normal blood pressure. In conclusion, the SHR Y chro mosome appears to increase the chronic sympathetic nervous system. A p otential mechanism could be a Y locus that influences chronic sympathe tic nervous system activity, which may reinforce neurohumoral factors and structural components of the Vessel wall, accelerating the develop ment of hypertension.