Pathogenesis of structural vascular changes in hypertension.

The pathogenic role of angiotensin II (ANG II), dietary sodium chloride, sympathetic activation, obesity and aldosterone in the development of structural vascular changes (SVCs) in hypertension is considered from three perspectives (criteria): their utility in predicting hypertension and its complications (predictability); the effect of their inhibition or removal on the reversal of SVCs (reversibility); and their ability to induce SVCs in experimental animals (reproducibility). Only ANG II meets all three criteria. Importantly, ANG II increases preglomerular vascular resistance by inducing structural changes in renal cortical resistance arteries and arterioles.

Why do treated hypertensives suffer strokes? An internist's perspective.

Despite widespread treatment of hypertension, stroke continues to be the third leading cause of death in the United States. Antihypertensive therapy is more effective in preventing hemorrhagic strokes than ischemic strokes. In order to understand the reasons why antihypertensive therapy is only partially successful in the eradication of ischemic strokes, differences in the pathogenesis and treatment of subtypes of stroke must be considered.

Understanding and Managing Isolated Systolic Hypertension in the Elderly.

In summary, ISHT in the elderly is a result of the interaction of increased systemic vascular resistance and of progressive arterial stiffening. The early return of reflected pulse wave may add to peak SBP in the ascending aorta and central arteries, thereby increasing LV systolic stress (afterload). Antihypertensive therapy has been shown to be effective in the prevention of strokes associated with ISHT.

Fecal hydrogen sulfide production in ulcerative colitis.

Objective: Sulfide, a product of sulfate-reducing bacteria, has been proposed to play an etiologic role in ulcerative colitis. Ulcerative colitis feces have increased numbers and activity of sulfate-reducing bacteria, but only modestly increased sulfide. However, fecal sulfide exists largely in the volatile, highly toxic H2S form that moves rapidly from feces to surrounding gas.