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C HAPTER 35 / Hypertension 801
contraction to maintain BP within normal limits. Over longer time identified gene coding for various components of the renin–
periods (hours to days), neurohumoral and direct renal regulation angiotensin–aldosterone system and their roles in the develop-
of vascular volume also play an important role in maintaining nor- ment of HTN. 21
mal BP. Baroreceptors in low-pressure components of the cardio- 4. Impaired vascular responsiveness, that is, impairments in vas-
vascular system such as the veins, atria, and pulmonary circulation cular dilation and increased vascular contraction, due to the
have a role in neurohumoral regulation of vascular volume. function of the endothelium, occurs in those individuals with
HTN occurs because there is an increase in cardiac output HTN. Oxidative stress is also a critical factor in both HTN and
and/or systemic vascular resistance. 31,32 It may be that either one atherogenesis. 33,34
or both are elevated. Because BP can be measured relatively easily 5. Insulin resistance may also play a role in the development of
and because it is not easy to measure cardiac output or systemic HTN. Insulin resistance may be the common factor that links
vascular resistance, we identify dysfunction of these variables as HTN, diabetes, and other metabolic abnormalities. The meta-
disorders of BP regulation. As discussion in several chapters of this bolic syndrome of abdominal obesity, increased BP, dyslipi-
book reveal, each of these variables, cardiac output and systemic demia, and insulin resistance with or without impaired glucose
vascular resistance, are themselves influenced by many factors. tolerance plus prothrombotic and proinflammatory states may
Given all the factors that can influence it, BP needs to be consid- place individuals at high cardiovascular risk.
ered as an extremely complex variable.
Secondary HTN
The Causes of HTN Secondary HTN affects between 5% and 10% of individuals with
HTN, and a large number of children younger than 10 years have
Despite decades of research, the main underlying cause of HTN
HTN due to a specific physiologic condition. In children younger
is unknown. However, HTN has been linked to a family history
than 10 years, the most common causes of persistent HTN are re-
and other factors, such as obesity, stress, excess sodium dysfunc-
nal disease and vascular problems such as coarctation of the aorta.
tion, and sympathetic nervous dysfunction, which may all con-
Common secondary causes of high BP in adults include chronic
tribute to HTN. It is highly likely that in the future it will be the
renal disease, renovascular disease, primary aldosteronism, and,
interaction of both genetic and environmental factors that play a
7
increasingly, sleep apnea. Display 35-1 summarizes the major
role in the hypotheses of the causes of HTN.
secondary causes of HTN in both children and adults. Aspects of
Primary HTN is the term used to describe 90% to 95% of all
diagnosis and management of some of the more common condi-
cases of HTN for which the cause is unknown. Secondary HTN,
tions are highlighted here.
which accounts for 5% to 10% of HTN cases, is linked to diseases
of the kidney, endocrine system, vascular system, lungs, and cen- Renal Parenchymal Disease. Chronic renal disease causes
tral nervous system. These conditions are described below. HTN and, conversely, HTN contributes to the development of
chronic renal disease. Three factors contribute to the development
Primary HTN
of HTN in those individuals with renal disease: loss of nephrons
The cause of primary HTN remains in question. BP is a complex
leading to retention of sodium, chloride, and water; decreased re-
variable involving mechanisms that influence cardiac output, sys-
lease of vasodilator substances such as nitric oxide; and activation
temic vascular resistance, and blood volume. HTN is caused by
of the renin–angiotensin system. NHANES III data indicates that
one or several abnormalities in the function of these mechanisms
70% of all patients with chronic renal disease have HTN. Aggres-
or the failure of other factors to compensate for these malfunc-
sive lowering of SBP may slow the progression of kidney disease,
tioning mechanisms. Currently, the genetic basis for rare types of
and clinicians must consider numerous options for treatment to
HTN has been identified, and there is hope that soon these dis-
reach goal BP.
coveries will lead to understanding of the cause or causes of most
HTN. Renovascular Disease. Renovascular HTN, found in 1%
Genetic factors and the environmental issues of obesity, stress, to 5% of all hypertensives, occurs when one or both of the renal
and excess sodium as well as sympathetic nervous system dysfunc- arteries are diseased, leading to decreased perfusion of the kidneys.
tion may all contribute to HTN. Several hypotheses are linked to The most common cause of renal artery stenosis is atherosclerosis,
understanding the cause of HTN and include the following: which leads to renal ischemia, release of renin from juxta-
glomerular cells of the kidney, and a secondary increase in BP. 35
1. Dysfunction of the autonomic nervous system imbalance may Diagnosis of renal artery stenosis is made on the basis of difficult
be a cause due to the inheritance of genes predisposing an in- to control BP or deterioration in renal function or electrolyte im-
dividual to increased sympathetic nervous activity. balance and through identification of an abdominal bruit by
2. Variations in renal sodium absorption also suggest that genes physical examination. This is followed by the either magnetic res-
involved in rare inherited forms of HTN may be related to mu- onance imaging or computed tomography and a renal angiogram
tations in several genes that increase one’s susceptibility to dis- with consideration of medical treatment, angioplasty, or surgery
orders of renal absorption of sodium, chloride, and water. To (which is the gold standard for severe renal artery stenosis). 36
date, genes accounting for the vast majority of salt-sensitive
HTN have not been identified. 21 Primary Hyperaldosteronism. Primary aldosteronism is a
3. Dysfunction of the renin–angiotensin–aldosterone system re- disease characterized by excess secretion of aldosterone, caused by
sults in an increase in renin–angiotensin–aldosterone activity an adrenocortical adenoma, adrenal hyperplasia, adrenal carci-
resulting in extracellular fluid volume expansion and systemic noma, or the cause may be unknown; in which case it is diag-
vascular resistance. Angiotensin II has also been shown to act nosed as idiopathic hyperaldosteronism. 37 A common form of
like a growth factor and a cytokine resulting in growth, differ- primary aldosteronism is a benign aldosterone producing ade-
entiation, and apoptosis in vascular tissues. Studies have also noma. With high levels of aldosterone there is retention of