Hypertension pathophysiology

Van Zwieten PA. Alpha-adrenoceptor blocking agents in the treatment of hypertension. In Laragh JH, Brenner BM, editors. Hypertension. Pathophysiology, diagnosis and management. 2nd ed. New York Raven Press 1995. p. 2917-36. 

Sealey J, Campbell G, Preibisz J. Hormone assays Renin, aldosterone, peripheral vein, and urinary assays. In Laragh J, Brenner B, eds. Hypertension pathophysiology, diagnosis, and management. New York Raven Press, 1990 1443-60,... 

Horl MP, Horl WH. Hemodialysis-associated hypertension Pathophysiology and therapy. Am J Kidney Dis 2002 39 227-244. 

Long after the discovery of renin in the late nineteenth century, the pathophysiology of arterial hypertension has been linked to the activation of vasoactive and salt-retaining hormones the neuroendocrine hypothesis has indeed been the base of a widely used paradigm (vaso-constriction/volume-dependent hypertension) to explain hypertensive pathophysiology and characterize different clinical presentations (Laragh, 1973 Johnson et al, 2005). 

Frohlich ED (1977) Essential hypertension. Pathophysiological mechanisms and therapy. Arch Intern Med 137 772-775... 

The kallikrein-kinin system as a regulator of cardiovascular and renal function, in Hypertension, Pathophysiology, Diagnosis and Management, 2nd edn (eds J.H. Laragh and B.M. Breimer), Raven Press Ltd., New York, NY, pp. 983-999. 

The pathophysiology of primary hypertension is heterogeneous, but ultimately exerts its effects through the two primary determinants of blood pressure cardiac output and peripheral resistance. 

BP, blood pressure CCB, calcium channel blocker agent DBP, diastolic blood pressure SBP, systolic blood pressure. (Adapted from JNC 7 Modified from Saseen JJ, Carter BL. Hypertension. In DiPiro JT, Talbert RL, Yee GC, et al, (eds.) Pharmacotherapy A Pathophysiologic Approach. 6th ed. New York McGraw-Hill 2005 194, with permission.)... 

The pathophysiologic mechanisms of portal hypertension and of cirrhosis itself are entwined with the mechanisms of ascites (Fig. 19-3). Cirrhotic changes and the subsequent decrease in synthetic function lead to a decrease in production of albumin (hypoalbuminemia). Albumin is the major intravascular protein involved in maintaining oncotic pressure in the vascular system low serum albumin levels and increased capillary permeability allow fluid to leak from the vascular space into body tissues. This can result in peripheral edema, ascites, and fluid in the pulmonary system. The obstruction of hepatic sinusoids and... 

The vascular endothelium produces a number of substances that are released basally into the blood vessel wall to alter vascular smooth muscle tone. One such substance is endothelin (ET-1). Endothelin exerts its effects throughout the body, causing vasoconstriction as well as positive inotropic and chronotropic effects on the heart. The resulting increases in TPR and CO contribute to an increase in MAP. Synthesis of endothelin appears to be enhanced by many stimuli, including Ag II, vasopressin, and the mechanical stress of blood flow on the endothelium. Synthesis is inhibited by vasodilator substances such as prostacyclin, nitric oxide, and atrial natriuretic peptide. There is evidence that endothelin is involved with the pathophysiology of many cardiovascular diseases, including hypertension, heart failure, and myocardial infarction. Endothelin receptor antagonists are currently available for research use only. 

Cirrhosis results in elevation of portal blood pressure because of fibrotic changes within the hepatic sinusoids, changes in the levels of vasodilatory and vasoconstrictor mediators, and an increase in blood flow to the splanchnic vasculature. The pathophysiologic abnormalities that cause it result in the commonly encountered problems of ascites, portal hypertension and esophageal varices, HE, and coagulation disorders. 

SR. Their elucidation may be of relevance to our understanding of alterations in SR function in pathophysiological processes, such as hypertension and pre-term labour. 

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