Pressor substances (vasoconstrictors)
This group of substances causes spasm of the smooth musculature of the vascular wall, 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 the concentration of the substance in the blood:
- Heart: exerts a pronounced stimulating effect, manifested by stronger and more frequent heart contractions.
- Abdominal, pulmonary, and cutaneous vessels: causes sustained constriction.
- Skeletal muscle arterioles: demonstrate a dose-dependent response. At high epinephrine concentrations, the $\alpha$-adrenergic effect prevails, causing vessel lumen narrowing. At low concentrations, $\beta$-adrenoceptors are activated, leading to vasodilation (depressor effect).
Vasopressin A neurohypophyseal hormone. Its vascular effect consists primarily in the constriction of arterioles and capillaries.
Angiotensin II (a component of the renin-angiotensin system) Possesses a potent pressor effect, which is realized at several levels simultaneously:
- Hemodynamic effect: direct and very pronounced vasoconstrictor action, naturally 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) concentration values, it is able to enhance the influence of the sympathetic nervous system on the heart and vascular bed.
Depressor substances (vasodilators)
Depressor agents generally have a pronounced local effect on the vascular bed, causing its dilation and improving tissue perfusion.
Acetylcholine Released from the endings of all parasympathetic nerve fibers, as well as from sympathetic vasodilators. The main target of this neurotransmitter is small arteries. Acetylcholine dilates their lumen, and this mechanism is closely linked to the formation of nitric oxide (NO) in the vascular wall.
Histamine Another potent tissue factor whose target is capillaries. Histamine exposure leads to preferential dilation of the capillary bed.
Kinin and its effect on hemodynamics
Kinins (e.g., bradykinin and lysyl-bradykinin) are peptides that participate in the complex regulation of blood pressure, invariably leading to its decrease. Their action consists of two major groups of effects:
- Vascular effects: kinins cause dilation of precapillary sphincters and small arterial vessels. In addition, they increase venous return and enhance the shunting of arterial blood into the venous bed bypassing capillaries—through arteriovenous anastomoses.
- Renal effects: kinins significantly increase renal blood flow and alter vascular wall permeability in the kidneys. This leads to increased urinary excretion of water, as well as sodium ($Na^+$), potassium ($K^+$), and chloride ($Cl^-$) ions.
Endothelial factors and prostaglandins
An extremely important role in vascular autoregulation is played by substances synthesized by the endothelium itself, as well as lipid mediators.
Prostacyclin Synthesized directly within the blood vessel wall. It causes relaxation of vascular smooth muscle cells using two parallel mechanisms:
- Stimulation of nitric oxide (NO) production.
- Activation of the enzyme adenylate cyclase, which entails an increase in the intracellular formation of cyclic adenosine monophosphate (cAMP).
Prostaglandins By their chemical nature, they are an extensive group of unsaturated fatty acids. They are localized in various tissues of the body, including the lungs, brain, kidneys, and liver. The chemical classification of prostaglandins implies their division into three main groups depending on the number of unsaturated bonds in the molecule.
Briefly: answers to topical questions
Which vasoactive substances are synthesized directly by the vascular endothelium?
The vascular endothelium releases two groups of vasoactive substances. Vasodilators: nitric oxide (NO), prostacyclin, endothelium-derived hyperpolarizing factor. NO diffuses into vascular smooth muscle cells, activates guanylate cyclase, and increases cGMP levels, leading to relaxation and dilation of the vessel. Prostacyclin causes vascular smooth muscle relaxation by stimulating NO production and activating adenylate cyclase with an increase in cAMP. Vasoconstrictor substances released by the endothelium: endothelin, superoxide anion, prostanoids, angiotensin II.
How does histamine affect capillaries and vascular wall permeability?
Histamine predominantly dilates capillaries and increases vascular permeability. In microcirculation, it increases capillary permeability; as a biologically active substance, histamine increases interendothelial gaps, leading to fluid egress from microvessels into the interstitium. In allergies and inflammation, this manifests as vasodilation, increased vascular wall permeability, edema, redness, and local temperature elevation.
How do various classes of prostaglandins (PGE, PGF) affect blood vessel tone?
Different classes of prostaglandins have varying effects on vascular tone and other smooth muscle functions.
| Prostaglandin class | Effect on vascular tone and smooth muscle |
|---|---|
| Group E (PGE, PGE2) | Cause arteriolar dilation (vasodilation) and a decrease in blood pressure. |
| Group F (PGF, PGF2α) | Stimulate intestinal smooth muscle contraction and initiate labor activity. Their direct pressor or depressor effect on blood vessels is not described in the literature. |
What factors stimulate renin secretion by the renal juxtaglomerular apparatus?
Renin secretion by the renal juxtaglomerular apparatus is stimulated in response to hemodynamic deterioration and changes in electrolyte composition. The main stimulating factors:
- Renal ischemia and decreased renal blood flow (in heart failure or thrombosis).
- Decreased blood pressure in the afferent arteriole and systemic arterial pressure.
- Increased concentration of sodium ions (Na+) in the urine of the distal convoluted tubule (excitation of macula densa osmoreceptors).
- Excitation of the sympathetic nervous system (release of norepinephrine and epinephrine acting on $\beta_1$-adrenoceptors).
What are the main humoral pressor factors of the blood, apart from epinephrine and angiotensin II?
Aside from epinephrine and angiotensin II, vasoconstrictor/pressor factors confirmed by sources include: vasopressin (ADH)—primarily constricts arterioles and capillaries; catecholamines, including norepinephrine—belong to endogenous BAS with vasoconstrictor action, and a massive release of epinephrine and norepinephrine is accompanied by a sharp increase in blood pressure; endothelin—an endogenous BAS with a potent vasoconstrictor effect; thromboxane A2—causes vasoconstriction and stimulates platelet aggregation; superoxide anion and prostanoids—indicated among vasoconstrictor substances released by the endothelium.
Pressor (constrictor) factors can be remembered by the rule "EAV": Epinephrine, Vasopressin, Angiotensin II.
Class and exam questions
How does adrenaline affect skeletal muscle vessels?
The effect strictly depends on the dose. At high concentrations, epinephrine causes constriction of muscle vessels, and at low concentrations—their dilation.
Through what mechanism does prostacyclin relax the vascular wall?
Prostacyclin stimulates the production of nitric oxide (NO) and activates adenylate cyclase, which increases cAMP levels in smooth muscle cells.
How do kinins lower blood pressure?
Blood pressure reduction is achieved through the dilation of small arteries, blood shunting via anastomoses, and also due to increased renal excretion of water and electrolytes.
What else to study on this topic
- Interaction of aldosterone and angiotensin II in BCC regulation
- The role of nitric oxide (NO) as a universal vasodilator
- Mechanisms of arteriovenous anastomoses during kinin action
- Differences between $\alpha$- and $\beta$-adrenergic effects of adrenaline
- Classification of prostaglandins by the number of unsaturated bonds
Master the entire topic in the "Physiology" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Humoral factors of vascular regulation" and 4,128 more pages of the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 114 video lessons on the subject
Other topics in "Vascular Bed Hemodynamics"
Free video lessons: PhysiologyShort lessons with study notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.