LONG-TERM CONTROL OF BLOOD PRESSURE

Although the sympathetic nervous system, through the sinoaortic baroreceptor reflex, plays a primary role in the rapid (minutes to hours) regulation of blood pressure, it appears to be less important in the long-term control of arterial pressure than neuroendocrine factors. The probable method for the long-term control of arterial pressure is the much slower-acting fluid volume regulation, with the hypothesized mechanism being renal pressure diuresis–natriuresis.

Although blood volume is not directly linked to arterial pressure, long-term arterial blood pressure control is based on the idea that arterial pressure is maintained at a level required by the kidneys to excrete a volume of urine approximately equivalent to the daily fluid intake (minus extrarenal fluid losses). The kidneys sense a change in blood volume through the arterial pressure.
That arterial pressure and not fluid volume is sensed is demonstrated in disease processes associated with a combination of increased extracellular volume and decreased arterial pressure (e.g., heart failure, cirrhosis with ascites). In these cases, the kidneys retain fluid despite expanded fluid volume.

Based on this hypothesis, an increase in arterial pressure as a result of increased systemic vascular resistance would cause an increase in sodium and water excretion. As long as sodium and water intake remained stable, the enhanced excretion would decrease extracellular volume and blood volume, and arterial pressure would decrease. According to this mechanism, an increase in systemic vascular resistance would not cause a long-term increase in arterial pressure unless renal function was impaired.

Renal Excretion of Sodium Chloride and Water
Despite the putative primacy of the renal diuresis–natriuresis mechanism in the long-term control of blood pressure, a hypothesis receiving some support is that arginine vasopressin and angiotensin II provide long-term feedback to the central nervous system. In addition, neural and hormonal factors modulate the renal diuresis–natriuresis response.

For example, a decrease in sodium intake stimulates renin activity, which leads to the generation of angiotensin II. An increase in angiotensin II decreases renal blood flow and the glomerular filtration rate, which indicates a shift of the pressure–natriuretic response (i.e., increased response to decreased sodium). Thus, angiotensin II appears to have an important role in the long-term modulation of renal function and the control of blood pressure.

Basal Tone
All arterioles exhibit a basal level of vasoconstriction or tone. Basal tone, which is the intrinsic level of vascular tone, is independent of neural or humoral influences and serves as the baseline around which neural or humorally mediated vasoconstriction or vasodilation occurs. Basal tone varies among organs; it is lowest in the kidneys and highest in the skeletal muscles, heart, and brain.

The maintenance of arteriolar tone through tonic rhythmic vasoconstriction is essential for the maintenance of blood pressure. For example, it is estimated that if this basal myogenic tone were eliminated, a minimal cardiac output of 60 to 75 L/min would be required to maintain a normal blood pressure.

In contrast, if the sympathetic input associated with resting tone were withdrawn, the blood pressure would decrease only from 100 to 86 mm Hg. This small decrease in blood pressure occurs because the vascular bed with the highest resting tone (skeletal muscle) normally receives only 15% of the cardiac output.