Patients with arterial
hypertension and no definable cause are said to have primary, essential, or idiopathic
hypertension.
Undoubtedly, the primary
difficulty in uncovering the mechanism(s) responsible for the hypertension in
these patients is attributable to the variety of systems that are involved in
the regulation of arterial pressure-peripheral and / or central adrenergic, renal,
hormonal and vascular-and to the complexity of the relationships of these systems
to one another.
Several abnormalities have been described in patients
with essential hypertension, often with a claim that one or more of these are
primarily responsible for the hypertension.
While it is still uncertain
whether these individual abnormalities are primary or secondary, varying expressions
of a single disease process or reflective of separate disease entities, the accumulating
data increasingly support the latter hypothesis.
Therefore, just as
pneumonia is caused by a variety of infectious agents, even though the clinical
picture observed may be similar, so essential hypertension likely has a number
of distinct causes.
Thus the distinction between primary and secondary
hypertension has become blurred, and the approach to both the diagnosis and therapy
of hypertensive patients has been modified.
For example, as a group of
patients with essential hypertension is separated into a distinct suset(eg., low-renin
essential hypertension), such patients have not been reclassified as having a
form of secondary hypertension but rather remain in the essential hypertensive
group.
Those individuals with a specific structural organ defect responsible
for hypertension are defined as having a secondary form of hypertension. In contrast,
individuals who may have generalized functional abnormalities causing their hypertension,
even if discrete are defined as having essential hypertension.
Heridity:
Genetic factors have long been assumed to be important in the genesis
of hypertension. Data supporting this view can be found in animal studies as well
as in population studies in humans.
One approach has been to assess the
correlation of blood pressure within families. From these studies the minimum
size of the genetic factor can be expressed by a correlation coefficient of approximately
0.2.
However, the variation in the size of the genetic factor in different
studies reemphasizes the likely heterogeneous nature of the essential hypertensive
population.
Additionally, most studies support the concept that the inheritance is probably
multi-factorial or that a number of different genetic defects each have as one
of their phenotypic expressions an elevated blood pressure.
Finally,
monogenic defects have now been reported which have as one of their consequences
an increased arterial pressure, e.g glucocorticoid-remedial aldostrenism.
Environment:
A number of environmental factors have been specifically implicated in the development
of hypertension, including salt intake, obesity, occupation, alcohol intake, family
size and crowding.
These factors have all been assumed to be important
in the increase in blood pressure with age in more affluent societies, in contrast
to the decline in blood pressure with age in more primitive cultures.
Salt
Sensitivity:
The environmental factor which has received the greatest
attention is salt intake. Even this factor illustrates the heterogenous nature
of the essential hypertensive population in that the blood pressure in only approximately
60 percent of hypertensives is particularly responsive to the level of sodium
intake.
The cause of this special sensitivity to salt varies, with primary
aldosteronism, bilateral renal artery stenosis, renal parenchymal disease, or
low rennin essential hypertension accounting for about half the patients.
In the remainder, the pathophysiology is still uncertain, but recent postulated
contributing factors include chloride, calcium a generalized cellular membrane
defect, insulin resistance and nonmodulation.
Role
of rennin: Renin is an enzyme secreted by the juxtaglomerular cell of the kidney
and linked with aldosterone in a negative feedback loop.
While a variety
of factors can modify this secretion, the primary determinant is the volume status
of the individual, particularly as related to changes in dietary sodium intake.
The
end product of the action of rennin on its substrate is the generation of the
peptide angiotension II. The response of target tissues to this peptide is uniquely
determined by the prior dietary electrolyte intake.
For example, sodicum
intake normally modulates adrenal and renal vascular responses to angiotensin
II. With sodium restriction, adrenal responses are enhanced and the renal vascular
responses reduced.
Sodium loading has the opposite effect.
The range of plasma rennin activities observed in hypertensive subjects is more
broad than in normotensive individuals. Thus some hypertensive patients have been
defined as having low-renin and others as having high rennin essential hypertension.
| Clinical
assessments and investigations involved in Hypertension | Hypertension
- Clinical presentation of target organs | Causes
of Secondary Hypertension | Treating
Hypertension Clinically |
