When most of us think of the regulation of arterial pressure, we almost immediately call to mind the carotid sinus reflex. The basic mechanism is the following: the carotid sinuses, along with the aortic arch and some of the other large arteries of the chest and neck, are supplied with stretch receptors called baroreeeptors. A rise in arterial pressure elicits impulses from the baroreeeptors; these in turn depress sympathetic stimulation of the circulation, thus returning the arterial pressure toward normal. Nothing could be simpler. But, also, for longterm regulation of arterial pressure, nothing could probably be further from the truth.
As a departure point to discuss longterm arterial pressure regulation, we can note that almost every clinician has been impressed by the strong relationship between arterial pressure and body-fluid balance. For instance, in patients who tend to have unstable pressures, a change in the intake of salt and water is almost always associated with a marked change in arterial pressure as well. Or any abnormality of kidney function that causes retention of water and salt will also be accompanied by a rise in arterial pressure. To control your pressure and spend little money on purchase you may buy Plendil via Canadian Health&Care Mall.
Therefore, this paper will be concerned primarily with these clinical observations, and we will make an attempt to show that the clinical observations arc almost certainly far more prophetic of longterm pressure regulation than has been the simplistic viewpoint that arterial pressure is controlled primarily by nervous reflex mechanisms.
The concept that the kidney’s ability to excrete water and salt is in some way inextricably bound with pressure control and with hypertension is a very old one—indeed, probably one of the oldest concepts of pressure control. It derives from the fact that hemorrhage causes a fall in arterial pressure and at the same time often completely blocks renal output of water and salt; the subsequent retention of fluid by the kidneys causes the blood volume to return to normal and the pressure likewise to return to normal.
On the other hand, it has been much more difficult to show that fluid volume plays a significant role in hypertension. But recent critical studies show that the renal-fluid volume mechanism for pressure regulation is a slowly acting system, the effects of which are almost impossible to demonstrate in acute experiments on pressure regulation. Therefore, it is easy to understand why its importance has long been overlooked and why this mechanism of pressure control has actually fallen into obscurity. It is our hope in this discussion to dispel this obscurity and in so doing to emphasize the extreme importance of the renal-body fluid mechanism for determining very precisely the longterm basic arterial pressure level.