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  • Title: [Cardiovascular alpha-, beta 1- and beta 2-adrenoceptor functions in neurogenic orthostatic hypotension].
    Author: Tamura N, Shimazu K, Yamamoto T, Maeda A, Hamaguchi K.
    Journal: Rinsho Shinkeigaku; 1995 Oct; 35(10):1120-4. PubMed ID: 8821496.
    Abstract:
    It has been believed that patients with neurogenic orthostatic hypotension (NOH) usually develop denervation supersensitivity of cardiovascular alpha-, beta 1- and beta 2-adrenoceptors, because the majority studies have shown augmented cardiovascular responses to intravenously given noradrenaline (NA) or isoprenaline (IP) in these patients. This view, however, leaves room for discussion. First, drugs were administered by means of drip infusion method in most of the previous studies. Since this method necessarily provokes baroreflex, which is buffering fluctuations in blood pressure and heart rate, the results may reflect diminished baroreflex rather than denervation supersensitivity. Second, adrenoceptor functions are modulated by multiple factors, such as ageing, thyroid hormone and chronic inflammation. It is, thus, inappropriate to explain the whole picture of functional change in adrenoceptors by the denervation mechanism only. In order to look over the cardiovascular adrenoceptor functions in NOH, we performed bolus infusion tests of NA and IP on the patients. The subjects comprised 7 cases of NOH with pre-ganglionic sympathetic deficit (NOH-I), 6 cases with post-ganglionic deficit (NOH-II) and 15 healthy controls. NOH-I group included 6 patients with multiple system atrophy and one with Parkinson disease, while NOH-II group consisted of 3 patients with idiopathic orthostatic hypotension (pure autonomic failure) and 3 with diabetic autonomic neuropathy. Both NA and IP infusion tests were carried out under the continuous measurement of blood pressure and heart rate. In NA test, different bolus doses (0.01, 0.02, 0.05 and 0.1 microgram/kg) of NA were intravenously administered, and a degree of subsequent rise in mean blood pressure was used as an index for alpha-adrenoceptor function. IP test was performed in the same manner, and an increase in heart rate and a fall in mean blood pressure in response to the drug (0.001, 0.002 and 0.005 microgram/kg) were measured as indices for beta 1- and beta 2-functions, respectively. A rise in blood pressure following the administration of any dose of NA did not statistically differ among three groups. An increase in heart rate in IP test was generally lower in both NOH groups, and a significant difference was obtained between NOH-I and control when a given dose was 0.005 microgram/kg) (p < 0.02). A fall in blood pressure in IP test was significantly greater in NOH-I compared to control when doses were 0.002 and 0.005 microgram/kg (p < 0.02 and 0.01, respectively). It was also greater in NOH-II than in control when a dose was 0.002 microgram/kg (p < 0.01). In disagreement with most of the previous studies, the present results suggest that alpha-adrenoceptor function is hardly altered, beta 1-function is suppressed, and beta 2-function is augmented in NOH.
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