Bloodpressureisdeterminedbyvascularresistanceandcardiacoutput.
Vascularresistanceisregulatedatthelevelofthearterioles,influencedbyneuralandhormonalinputs.
Cardiacoutputisdeterminedbyheartrateandstrokevolume,thelatterofwhichisstronglyinfluencedbybloodvolume.Bloodvolumeinturnisregulatedmainlybyrenalsodiumexcretionorresorption.
Renin,amajorregulatorofbloodpressure,issecretedbythekidneysinresponsetodecreasedbloodpressureinafferentarterioles.Inturn,renincleavesangiotensinogentoangiotensinI;subsequentperipheralcatabolismproducesangiotensinII,whichregulatesbloodpressurebyincreasingvascularSMCtoneandbyincreasingadrenalaldosteronesecretion,whichconsequentlyincreasesrenalsodiumresorption.
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Fig. 10.4 Interplayofrenin,angiotensin,aldosterone,andatrialnatriureticpeptideinbloodpressureregulation(seetext).
Hypertension is a major health problem in the developed world. Although it occasionally manifests in an acute aggressive form, high blood pressure is typically asymptomatic for many years. This insidious condition has been dubbed essential hypertension, so called because the gradual age-associated rise in blood pressure was considered “essential” for normal perfusion of endorgans such as the brain. However, such increases are neither essential nor benign; besides increasing the risk for stroke and atherosclerotic coronary heart disease, hypertension can lead to cardiac hypertrophy and heart failure (hypertensive heart disease; see Chapter 11), aortic dissection, multi-infarct dementia, and renal failure. While the molecular pathways of blood pressure regulation are reasonably well understood, the mechanisms leading to hypertension in the vast majority of affected individuals remain unknown. The accepted wisdom is that “essential hypertension” results from the interplay of several genetic polymorphisms (which individually might be inconsequential) and environmental factors, which conspire to increase blood volume and/or peripheral resistance.
Like height and weight, blood pressure is a continuously distributed variable; moreover, detrimental consequences increase continuously as the pressure rises, with no rigidly defined threshold dependably predicting total safety. Nevertheless, sustained diastolic pressures greater than 90 mm Hg or sustained systolic pressures in excess of 140 mm Hg are reliably associated with an increased risk for atherosclerosis and are therefore used as cutoffs in diagnosing hypertension in clinical practice. By these criteria, over 25% of individuals in the general population are hypertensive. As noted however, these values are somewhat arbitrary, and in patients with other cardiovascular risk factors (e.g., diabetes), lower thresholds may be applicable.
The prevalence of pathologic effects of high blood pressure increases with age and is also higher in African Americans. Without appropriate treatment, some 50% of hypertensive patients die of ischemic heart disease (IHD) or congestive heart failure, and another third succumb to stroke. Reduction of blood pressure dramatically reduces the incidence and clinical sequelae (including death) of all forms of hypertension-related disease. Indeed, treatment of asymptomatic hypertension constitutes one of the few instances in which “preventive medicine” has a major demonstrated health benefit.
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A small percentage of hypertensive patients (approximately 5%) present with a rapidly rising blood pressure that, if untreated, leads to death in within 1 to 2 years. Such malignant hypertension usually is severe (i.e., systolic pressures over 200 mm Hg or diastolic pressures over 120 mm Hg) and frequently is associated with renal failure and retinal hemorrhages, with or without papilledema. It can arise de novo but most commonly is superimposed on preexisting benign hypertension.