Pressor Substances (Vasoconstrictors)
This group of substances causes contraction of vascular smooth muscle, leading to an increase in blood pressure. The main pressor factors include:
Epinephrine A hormone secreted by the adrenal medulla. Its effects depend on the target organ and its concentration in the blood:
- Heart: Exerts a pronounced positive inotropic and chronotropic effect, increasing the force and rate of cardiac contractions.
- Abdominal, pulmonary, and cutaneous vessels: Causes sustained vasoconstriction.
- Skeletal muscle arterioles: Exhibit a dose-dependent response. At high concentrations, the $\alpha$-adrenergic effect predominates, causing vasoconstriction. At low concentrations, $\beta_2$-adrenergic receptors are activated, leading to vasodilation (depressor effect).
Vasopressin (ADH) A posterior pituitary hormone. Its vascular effect is primarily the constriction of arterioles and capillaries.
Angiotensin II (Component of the Renin-Angiotensin System) Exerts a potent pressor effect implemented at multiple levels:
- Hemodynamic effect: Direct and very pronounced vasoconstriction, systematically leading to an increase in both systolic and diastolic blood pressure.
- Endocrine effect: Directly acts on the adrenal cortex, enhancing the secretion of aldosterone and glucocorticoids.
- Neurogenic effect: Even at minimal (threshold) concentrations, it enhances the influence of the sympathetic nervous system on the heart and vasculature.
Depressor Substances (Vasodilators)
Depressor agents typically exert a pronounced local effect on the vascular bed, causing vasodilation and improving tissue perfusion.
Acetylcholine Released from the terminals of all parasympathetic nerve fibers, as well as sympathetic vasodilators. The primary target of this neurotransmitter is small arteries. Acetylcholine dilates their lumen, a mechanism closely linked to the generation of nitric oxide (NO) within the vascular wall.
Histamine Another potent tissue factor targeting capillaries. Histamine exposure leads to predominant dilation of the capillary bed.
Kinins and Their Hemodynamic Effects
Kinins (e.g., bradykinin and lysyl-bradykinin) are peptides involved in the complex regulation of blood pressure, consistently leading to its reduction. Their action consists of two major groups of effects:
- Vascular effects: Kinins cause dilation of precapillary sphincters and small arterial vessels. Additionally, they increase venous return and shunt arterial blood directly into the venous system bypassing capillaries via arteriovenous anastomoses.
- Renal effects: Kinins significantly increase renal blood flow and alter the permeability of the renal vascular wall. This leads to increased urinary excretion of water, as well as sodium ($Na^+$), potassium ($K^+$), and chloride ($Cl^-$) ions.
Endothelial Factors and Prostaglandins
Substances synthesized by the endothelium itself, along with lipid mediators, play a crucial role in vascular autoregulation.
Prostacyclin Synthesized directly in the blood vessel wall. It causes relaxation of vascular smooth muscle cells via two parallel mechanisms:
- Stimulation of nitric oxide (NO) production.
- Activation of adenylyl cyclase, leading to increased intracellular formation of cyclic adenosine monophosphate (cAMP).
Prostaglandins Chemically, these are a broad group of unsaturated fatty acids. They are localized in various body tissues, including the lungs, brain, kidneys, and liver. The chemical classification of prostaglandins involves their division into three main groups based on the number of unsaturated bonds in the molecule.