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Angiotensin-catecholamine effects in rats remain hypothesis-generating; leaves open any clinical relevance to human hypertension.
Several recent investigations have presented indirect evidence that angiotensin stimulates the release of adrenal medullary catecholamines. The following work was undertaken to elucidate the angiotensin action on the adrenal medulla and effect of myocardial catecholamines through observations of the changes in the adrenal and myocardial catecholamines caused in the rat by angiotensin injection. An injection of 0.5μg/kg body weight of angiotensin into the coccygeal vein brought about a significant decrease in adrenal noradrenaline after 3 minutes and also a significant decrease in adrenal adrenaline after 10 minutes. On the other hand, myocardial noradrenaline rose significantly. These results show that angiotensin is an effective stimulant for adrenal medullary cate-cholamines, and also angiotensin causes an increase in myocardial catecholamine, or noradrenaline, in particular.
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Minoru Kawabata (1970) studied this question.
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