Spontaneously hypertensive rat Y chromosome increases indexes of sympathetic nervous system activity.
Previous studies from our laboratory have demonstrated that the Y chromosome from the spontaneously hypertensive rat (SHR) is responsible for a significant portion of the elevated blood pressure and also produces an earlier pubertal rise in plasma testosterone. We performed the following studies to determine whether the SHR Y chromosome raises blood pressure by sympathetic nervous system responses as measured by adrenal 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, and aortic telemetry (Data Sciences); acute (air stress) and chronic (territorial colony) social stressors were compared; blood was collected for determination of plasma catecholamines; and adrenal glands were analyzed at 15 weeks for catecholamines. Rats with the SHR Y chromosome had higher blood pressure and plasma norepinephrine than those with the normotensive Wistar-Kyoto (WKY) Y chromosome. However, the SHR Y chromosome did not significantly change responsiveness to acute or chronic stressors. Phentolamine and clonidine prevented the stress responses. Adrenal chromogranin A levels were elevated 37% and 40% and adrenal norepinephrine content 29% and 100% at 4 and 10 weeks of age, respectively, in rats with an SHR Y chromosome compared with WKY. Chemical sympathectomy normalized blood pressure in all strains and significantly reduced norepinephrine (36% to 41%) in all strains except in WKY, which already had a normal blood pressure. In conclusion, the SHR Y chromosome appears to increase the chronic sympathetic nervous system. A potential mechanism could be a Y locus that influences chronic sympathetic nervous system activity, which may reinforce neurohumoral factors and structural components of the vessel wall, accelerating the development of hypertension.
Ely
D
D
Department of Biology, University of Akron, Ohio 44325-3908, USA.
Caplea
A
A
Dunphy
G
G
Daneshvar
H
H
Turner
M
M
Milsted
A
A
Takiyyudin
M
M
D000311:Adrenal Glands / Q000737:chemistry; D000367:Age Factors; D000704:Analysis of Variance; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects / Q000235:genetics*; D053379:Chromogranin A; D002864:Chromogranins / Q000032:analysis; D003000:Clonidine / Q000494:pharmacology; D004298:Dopamine / Q000032:analysis; D004837:Epinephrine / Q000032:analysis; D006973:Hypertension / Q000235:genetics*; D008297:Male; D009638:Norepinephrine / Q000032:analysis; D010646:Phentolamine / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013312:Stress, Physiological / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000502:physiology*; D014998:Y Chromosome / Q000235:genetics*
D000959:Antihypertensive Agents; D053379:Chromogranin A; D002864:Chromogranins; D003000:Clonidine; D004298:Dopamine; D009638:Norepinephrine; D004837:Epinephrine; D010646:Phentolamine