Sympathetic Abnormalities in Human Hypertension

Champlain, Jacques de; Cousineau, Denis; Lapointe, Luc; Lavallée, Michel; Nadeau, Réginald; Denis, Gustave

doi:10.3109/10641968109033674

Cited by 16 publications

(4 citation statements)

References 30 publications

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“…However, others have found no evidence of increased sympathetic activity in borderline hypertensives (Henquet et al, 1981). In groups of hypertensive patients who have increased levels of circulating catecholamines, suggestive of an increased sympathoadrenal tone, studies of postural changes in circulating levels of norepinephrine, catecholamines, and epinephrine have led some researchers to postulate that the SNS hyperreactivity occurring in these hypertensive patients may be secondary to a decrease in the inhibitory PNS tone on sympathetic fibers (deChamplain et al, 1981).…”

Section: Physiological Variablesmentioning

confidence: 99%

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Genetic and familial factors in essential hypertension and related traits

Siervogel

1983

American J Phys Anthropol

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The health significance of essential hypertension (high blood pressure of undefined origin) is well established. It is a major factor contributing to coronary heart disease, stroke, and kidney failure. It directly affects about one in five Americans. Factors which are known to be associated with blood pressure include: body composition as it relates to overall mass and fat mass; physiological variables involving the sympathetic and parasympathetic nervous systems; biochemical variables such as renin, aldosterone, kallikrein, lipids, and lipoproteins, etc.; environmental variables such as sodium intake, heavy metals, and noise; and psychological variables involving personality type and mental stress.There is a definite, well-established genetic involvement in hypertension, but specific genetic mechanisms remain a mystery. Familial aggregation occurs for many of the associated traits listed above. For some, specific polymorphic major genes have been identified, but for others genetic factors are unidentified. Essential hypertension is undoubtedly a heterogeneous group of diseases with the common end result of elevated blood pressure. Because of its health significance, there is considerable interest in identifying genetic mechanisms resulting in essential hypertension. One area that currently shows some potential for the identification of a specific genetic mechanism is related to the transmembrane transport of sodium and potassium cations.A genetic component has long been suspected in essential hypertension, but a clear and definitive genetic mechanism has yet to be identified. Since there are many variables that can affect blood pressure, this review of the genetics of essential hypertension necessarily involves a discussion of related traits. Before focusing on the genetic and familial aspects of hypertension a description of the normal course of human blood pressure is presented and some of the traits related to it are discussed. NATURAL HISTORY OF BLOOD PRESSUREUntil recently, reports describing blood pressure patterns during the neonatal period were relatively few, largely because of the difficulty of accurately measuring blood pressure in infants by noninvasive techniques. The ultrasonic technique utilizing the Doppler effect greatly facilitated noninvasive systolic blood pressure determination in infants (McLaughlin et al., 1971). Accurate automatic methods are currently available using the oscillometric principal coupled with a microcomputer and a standard limb blood presure cuff (Friesen and Lichtor, 1981). Even in adults newer methods are being developed (Wolthuis et al., 1981).© 1983 Alan R. Liss, Inc. [Vol.26,1983 Systolic blood pressure tends to increase sharply during the first two weeks of life from a mean of 70 mmHg at 2 days to 84 mmHg at 2 weeks. It continues to increase at a slightly slower rate over the next 4 weeks to a mean of about 93 mmHg at 6 weeks (Earley et aI., 1980); from 6 weeks to 1 year af age there is little change in systolic pressure (deSwiet et aI., 1975(deSwiet et ...

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Section: Physiological Variablesmentioning

confidence: 99%

“…43 circulating levels of norepinephrine, catecholamines, and epinephrine have led some researchers to postulate that the SNS hyperreactivity occurring in these hypertensive patients may be secondary to a decrease in the inhibitory PNS tone on sympathetic fibers (deChamplain et al, 1981).…”

Section: Genetic Factors In Hypertensionmentioning

confidence: 99%

Genetic and familial factors in essential hypertension and related traits

Siervogel

1983

American J Phys Anthropol

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“…Therefore, the develop ment of new and effective antihypertensive drugs with different modes of action is still required. As is well known, vascular resistance is under the active control of sympathetic nerve fibers, and stimulation of a-adrenoceptors is primarily associated with vasoconstriction and a rise in arterial blood pressure [9,12,26], Based on the relative order of selectivities of agonists and antagonists that covers a wide spectrum, a-adrenoceptors have been classified into either the ai or cb subtype [27], The clinical efficacy of the selective ai-adrenoceptor antagonist, pra zosin, as an ideal antihypertensive agent has attracted renewed interest in a-adrenoceptor antagonists [4,23,25] as therapeutic agents and has contributed to the assess ment of the potential of this class of compounds for novel therapeutic indications.…”

Section: Dc-015 Prazosinmentioning

confidence: 99%

Antihypertensive and Hypolipidemic Effects of DC-015, a Novel, Potent and Specific α(1)-Adrenoceptor Antagonist: Comparison with Prazosin in Spontaneously Hypertensive Rats

Peng¹,

Shei²,

Chern³

et al. 1996

J Biomed Sci

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The hypotensive effect of DC-015, a newly synthesized quinazoline derivative, was investigated and compared with prazosin in spontaneously hypertensive rats (SHR). Intravenous administration of DC-015 and prazosin (both at 0.01, 0.05 and 0.1 mg/kg) induced a dose-dependent reduction of mean arterial pressure (MAP) which reached a maximal effect at 5 min after injection and persisted over 2 h in SHR. Furthermore, at higher doses DC-015 (0.1 mg/kg i.v. and 2.0 mg/kg orally, respectively) did not cause any significant changes in heart rate (HR); whereas the same doses of prazosin (0.1 mg/kg i.v. and 2.0 mg/ kg orally, respectively) produced a decrease in HR which seems to parallel the time course of the hypotensive response in SHR. DC-015 and prazosin attenuated pressor responses to phenylephrine (10 μg/kg) but failed to inhibit the pressor effects of angiotensin II (0.5 μg/kg) even at the maximal hypotensive dose (0.1 mg/kg). This observation indicates that DC-015 appears to exert its hypotensive effect through α(1)-adrenoceptor blockade. On the other hand, in SHR fed a high-fat-high-cholesterol (HF-HC) diet, oral administration of DC-015 and prazosin (both at 1.0 mg/kg, twice a day) for 4 weeks caused significant reductions in total plasma cholesterol (CE), low-density lipoprotein (LDL)-cholesterol and total plasma triglyceride (TG). DC-015 therapy also increased high-density lipoprotein (HLD)-cholesterol levels, thus the ratio of total plasma cholesterol to HDL-CE was improved. In contrast, prazosin did not significantly increase the HDL-CE level in this study. It is concluded that DC-015 decreased MAP, plasma CE, LDL-CE, plasma TG and increased HDL-CE levels. DC-015 may have therapeutic potential as a potent antihypertensive drug via the α(1)-adrenoceptor antagonist. Concurrently, DC-015 may thus hold some advantage for the reduction of two of the major risk factors, hypertension and hyperlipidemia, for cardiovascular diseases.

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“…under the active control of sympathetic nerve fibers (4)(5)(6). Numerous observationE have indicated that vasculatures contain twc subpopulations of a-adrenoceptors, i.e., al and a2-adrenoceptors mediating vasocon strictor responses to a-adrenoceptor agonise (7,8).…”

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confidence: 99%