Basal Tone and Local Autoregulation
The caliber of the vascular bed largely depends on basal tone, which is established by smooth muscle automacy and the stretching of elastic vessel walls by the pulse wave. This parameter is directly influenced by the high partial pressure of oxygen in arterial blood and the presence of $Ca^{2+}$ ions.
The endothelium plays an exceptional regulatory role by releasing biologically active substances:
- Vasodilators (widen the lumen): nitric oxide (NO), prostacyclin, endothelium-derived hyperpolarizing factor.
- Vasoconstrictors (narrow the lumen): endothelin, superoxide anion, prostanoids, angiotensin II.
Mechanism of NO Action: Nitric oxide diffuses into vascular smooth muscle cells, where it activates guanylyl cyclase (coupled to a G-protein). This leads to an increase in intracellular cyclic guanosine monophosphate (cGMP) and relaxation of the vessel wall.
Neural Regulation and Hemodynamic Reflexes
Central nervous regulation is based on the activity of the vasomotor center in the medulla oblongata, which has pressor and depressor regions. Changes in blood pressure trigger systemic reflexes:
- Depressor (Baroreceptor) Reflex: In response to a rise in blood pressure, firing from arterial baroreceptors increases. This causes reflexive inhibition of sympathetic center neurons—they stop sending signals to spinal preganglionic neurons, resulting in vasodilation.
- Bainbridge Reflex: The body's response to an increase in central venous pressure.
- Parin Reflex: An increase in pulmonary trunk pressure causes bradycardia, a drop in systemic blood pressure, and dilation of splenic vessels.
Features of Autonomic Innervation: Sympathetic stimulation generally causes vasoconstriction. However, there are exceptions: blood vessels of the brain, heart, lungs, and active skeletal muscles dilate during sympathetic activation. This is due to the presence of cholinergic fibers within sympathetic trunks that release acetylcholine (ACh). The physiological purpose is to preemptively supply oxygen to muscles and vital organs during rapid physical mobilization.
The parasympathetic system (vagus nerve) also has diverse effects: its fibers dilate pulmonary vessels (increasing blood flow), but constrict coronary vessels.
Influence of Blood Gases and Metabolic Products
Visceral systems are highly sensitive to metabolites and gases, though they respond differently depending on the organ.
Effect of Oxygen ($O_2$):
- In the myocardium and brain: Hypoxia (a drop in $O_2$) causes active and pronounced vasodilation.
- In the lungs: Alveolar hypoxia (due to disease or breathing $O_2$-poor gas mixtures) leads to simultaneous constriction of pulmonary arterioles. This is a protective mechanism that sharply increases pulmonary vascular resistance and pulmonary arterial pressure.
Effect of Carbon Dioxide ($CO_2$): In coronary vessels, high $CO_2$ concentrations produce a biphasic response: initial tone elevation due to central mechanisms, followed by a significant drop in pressure (vasodilation) due to local effects. In brain tissue, rising $CO_2$ dissociates into carbonic acid, releasing $H^+$ ions, which leads to vasodilation ($H^+$ ions themselves do not cross the blood-brain barrier easily, but $CO_2$ freely diffuses).
Metabolites and Ions: Coronary vasodilation is promoted by adenosine, bradykinin, prostaglandins, lactate, and NO. In skeletal muscles, local vasodilation during contraction is mediated by $K^+$ ions and phosphates. Adenosine is also a key factor in regulating cerebral blood flow—its levels rise during ischemia, hypoxemia, and hypotension.