Spontaneously hypertensive rats exhibit specific enhanced venous contraction to norepinephrine that cannot be explained by structural changes in venous smooth muscle.
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Venous norepinephrine hypersensitivity in hypertensive rat models merits mechanistic follow-up; leaves open relevance to human hypertension.
Jugular veins from normotensive rats respond to norepinephrine with a beta adrenergically-mediated relaxation, and thus provide a useful tissue for the examination of changes in venous responses to norepinephrine in hypertension. Jugular veins from spontaneously hypertensive rats did not relax to norepinephrine and in some tissues, a contraction occurred. After propranolol (10-6 M), norepinephrine contracted jugular veins from both groups. However, contraction to norepinephrine was greater in veins from spontaneously hypertensive rats. Enhanced contraction was specific to norepinephrine since maximal force developed to serotonin and potassium chloride was less in veins from spontaneously hypertensive rats. Thus structural changes in venous smooth muscle cannot explain the enhanced contraction to norepinephrine. Relaxation to isoproterenol, nitroglycerin or norepinephrine (after alpha adrenoceptor blockade with prazosin) was not decreased in jugular veins from spontaneously hypertensive rats in comparison to normotensive rats. Likewise, defective relaxation of portal veins was not apparent in this hypertensive model although a defect in relaxation was confirmed in
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Cohen et al. (1979) studied this question.
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