Human hypertension

Litton RP, Gharavi AG, Geller DA (2001) Molecular mechanisms of human hypertension. Cell 104 545—556... 

Casiglia, E., Paleari, C. D., Petucco, S., Bongiovi, S., Colangeli, G., Baccilieri, M. S., Pavan, L., Pernice, M., and Pessina, A. C., Haemodynamic effects of coffee and purified caffeine in normal volunteers A placebo-controlled clinical study. Journal of Human Hypertension 6, 95-99, 1992. 

Staessen J, Sartor F, Rods H, et al. 1991. The association between blood pressure, calcium and other divalent cations A population study. Journal of Human Hypertension 5 485-494. 

Butler R, Morris AD, Burchell B, Struthers AD. DD angiotensin-converting enzyme gene polymorphism is associated with endothelial dysfunction in normal humans. Hypertension 1999 33 1164-1168. 

Jeunemaitre X, Soubrier F, Kotelevt-sev YV, Lifton RP, Williams CS, Char-ru A, Hunt SC, Hopkins N, Williams RR, Lajouel J-M, Corvol P. Molecular basis of human hypertension role of an-giotensinogen. Cell 1992 71 169-180. 

Corvol P, Jeunemaitre X. Molecular genetics of human hypertension Role of angiotensinogen. Endocrine Rev 1997 18 662-677. 

Jeunemaitre, X., Soubrier, F., Kotelevtsev, Y. V., et al. (1992) Molecular-basis of human hypertension—role of angiotensinogen. Cell. 71, 169-180. 

Tank J et al Yohimbine attenuates baroreflex-mediated bradycardia in humans. Hypertension 2007 50 899. 

Shreenivas S, Oparil S The role of endothelin-1 in human hypertension. Clin Hemorheol Microcirc 2007 37 157. [PMID 17641406] Stauffer BL, Westby CM, DeSouza CA Endothelin-1, aging and hypertension. Curr Opin Cardiol 2008 23 350. [PMID 18520719]... 

Corvol, P. (1995). Liddle s syndrome heritable human hypertension caused by mutations in the Beta subunit of the epithelial sodium channel. J. Endocrinol. Invest., 18(7), 592-594. 

Mune T, Rogerson FM, Nikkila H, Agarwal AK, White PC. Human hypertension caused by mutations in the kidney isozyme of 11 P-hydroxysteroid dehydrogenase. Nature Genetics 10 1995 394-399. 

McCarron, D. A. 1983. Calcium and magnesium nutrition in human hypertension. Ann. Intern. Med. 98(Part 2), 800-805. 

From what has already been published, and from what is contained in this symposium, it is abundantly clear that at least the early period of the hypertension which develops after constriction of the main renal arteries of animals is of humoral origin. The difficulty has been, and still is, the direct application of what has been learned about experimental renal hypertension to the problem of the pathogenesis of human essential hypertension. Of the greatest importance would be the determination of the exact cause of the relatively long period of experimental hypertension and of human hypertension in which, up to the present time, the existence of a humoral mechanism has not been proved. 

Many other unidentified pressor materials have been isolated from organs and fluids (see von Euler, 20, for discussion). Some of them were probably simple amines, others epinephrinelike. They have been given a variety of names. Because of their non-specific nature and the manner of their extraction it seems unlikely that they are concerned in the development or maintenance of chronic human hypertension. 

The renal pressor mechanism—renin and hypertensin—acts in acute hypertension and in acute renal ischemic states, but apparently not in chronic hypertension. The other mechanisms shown to be active in chronic hypertension are vasoexcitor-vasodepres-sor material relationship pherentasin, a pressor substance found only in human hypertension amines resulting from the insufficient oxidation of amino acids, which are increased in human hypertension and norepinephrine (Sympathin E), which largely reproduces the hemodynamic picture of chronic hypertension. Most of the known pressor substances, with the notable exception of norepinephrine, come from disturbances of, or are extracted from, the kidneys. The large number of pressor substances which have been obtained suggests that many may represent different stages of metabolism of certain parent substances, and that their effectors may be fewer in number and simpler in structure. The chemical identification and purification of most of these substances leave much to be desired, and their phafmacology has in most cases been inadequately studied. The whole problem, however, may soon become simplified. 

Because of the many dissimilarities between human essential hypertension and experimental neurogenic hypertension, studies of the latter have been relegated to the background in recent years in favor of work on experimental renal hypertension, which much more closely resembles essential hypertension (Table I 11, 35, 64, 77). Nevertheless, a careful analysis of neurogenic hypertension is important as a basis for the recognition or exclusion of neurogenic factors in human hypertension. 

In summarizing evidence for the participation of deranged sympatho-adrenal ( neurogenic ) factors in human hypertension, it must be concluded that such factors have been conclusively demonstrated only in cases of pheochromocytoma, central nervous system trauma, and increased intracranial pressure. There is presumptive evidence that neurogenic factors may be important during the early, labile phases of essential hypertension and that the effects of this early sympatho-adrenal activity may lead to a persistent hypertension on a renal basis later in life. However, the development of hypertension through this or any other mechanism occurs only in individuals predisposed by some completely unknown, but probably hereditary, influence. 

At the present time, pheochromocytoma and intracranial lesions are the only causes of human hypertension which are definitely known to involve overactivity of the sympatho-adrenal system. However, presumptive evidence is accumulating to indicate that neurogenic factors may be involved in early essential hypertension, and it is possible that adequate adrenergic blockade early in the course of such hypertension may be effective in aborting its development. Only additional evidence regarding the etiology of essential... 

Malmqvist K, Kahan T, Edner M, Held C, Hagg A, Lind L, Muller-Brunotte R, Nystrom F, Ohman KP, Osbakken MD, Ostergem J. Regression of left ventricular hypertrophy in human hypertension with irbesartan. J Hypertens 2001 19 1167-1176. 

Howie AJ (1996) Benign essential hypertension and kidney damage a histopathologist s view, journal of Human Hypertension 10 691-694. 

British Heart Foundation Statistics Database (1998). Coronary Heart Disease Statistics 1998. London British Heart Foundation Cappuccio FP (1997). Ethnicity and cardiovascular risk variations in people of African ancestry and South Asian origin. Journal of Human Hypertension 11 571-576 Connor MD, Walker R, Modi G et aL (2007). Burden of stroke in black populations in sub-Saharan Africa. Lancet Neurology 6 269-278 Coull AJ, Lovett JK, Rothwell PM et al. (2004). Population based study of early risk of stroke after transient ischaemic attack or minor stroke implications for public education and organisation of services. British Medical Journal 328 326... 

Moriwaki H, Uno H, Nagakane Y et al. (2004). Losartan, an angiotensin n (ATI) receptor antagonist, preserves cerebral blood flow in hypertensive patients with a history of stroke. Journal of Human Hypertension 18 693-699... 

N. Fujiwara, T. Osanai, T. Kamada, T. Katoh, K. Takahashi and K. Okumura. Study on the Relationship Between Plasma Nitrite and Nitrate Level and Salt Sensitivity in Human Hypertension. Modulation of Nitric Oxide Synthesis by Salt Intake, Circulation 101 (2000) 856-864. 

Mene P, Pugliese F, Patrono C. The effects of nonsteroidal anti-inflammatory drugs on human hypertensive vascular disease. Semin Nephrol 1995 15(3) 244-52. 

Musso NR, Vergassola C, Pende A, Lotti G. Yohimbine effects on blood pressure and plasma catecholamines in human hypertension. Am J Hypertens 1995 8(6) 565-71. 

Celis H,Thijs L, Staessen JAet al. Interaction between nonsteroidal anti-inflammatory drug intake and calcium-channel blocker-based antihypertensive treatment in the Syst-Eur trial. Journal of Human Hypertension 2001 5 613-618. 

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