Composition and determinants of CBV
The constancy of the circulating blood volume is ensured by maintaining two basic components: a constant plasma volume and a stable formed element mass (primarily erythrocytes).
CBV is not an absolutely rigid constant—its value flexibly changes in response to external conditions and the functional needs of the organism:
- An increase in volume occurs during physical activity.
- A decrease in volume is physiologically observed at rest, during sleep, and at high temperatures due to fluid loss with sweat.
- Influence of orthostasis: upon a abrupt transition to a vertical position, the volume briefly decreases as part of the blood is pooled in the capacitance veins of the lower extremities and abdominal cavity.
Afferent link: how the body senses changes
Deviation of CBV from the metabolic optimum is instantly detected by a complex receptor apparatus:
- Volumoreceptors (volume receptors): assess the degree of blood filling in the heart itself and the vascular bed.
- Baroreceptors: respond to pressure changes and wall stretch. Their main localization is in reflexogenic zones (aortic arch and sinocarotid region).
- Osmoreceptors: are inevitably involved, as blood volume is inextricably linked to water-electrolyte balance.
- Chemoreceptors: are activated when tissue blood supply deteriorates and pH shifts occur (from the normal 7.35–7.40).
Signals from receptors are transmitted via afferent pathways (including the depressor and sinocarotid nerves) to central structures. In the medulla oblongata, the vasomotor center is activated, neurohumoral self-regulation is triggered in the hypothalamus, and the cerebral cortex forms higher behavioral responses.
Effector mechanisms of regulation
To return CBV to normal (e.g., during hemorrhage or plasma loss), the body engages effector mechanisms. They are divided into fast and slow.
Fast mechanisms (hemodynamics and redistribution):
- Change in cardiac output: compensatory alteration of heart rate and contraction force.
- Change in vessel lumen: venoconstriction occurs primarily (reducing the capacity of veins storing >60% of blood), and only then do arteries constrict.
- Mobilization of blood reservoirs: release of additional blood from the liver, spleen, lungs, and skin.
- Transcapillary exchange: redistribution of fluid between the interstitium and blood vessels based on the difference in hydrostatic and oncotic pressures.
Slow mechanisms:
- Water balance and excretion: regulation of renal function (diuresis) and sweat gland activity.
- External link (drinking behavior): the hypothalamus forms the sensation of thirst and motivation to seek water.
- Hematological processes: enhancement of blood formation (erythropoiesis) and control of blood destruction (hemolysis).
Endocrine control: antagonist hormones
Humoral regulation relies on the balance of fluid-conserving and fluid-excreting systems.
Fluid retention systems:
- Hypothalamic-pituitary system: increases the secretion of vasopressin (ADH), which inhibits renal water excretion.
- RAAS (renin-angiotensin-aldosterone system): increases the reabsorption of $Na^+$ ions and water, increasing CBV. Angiotensin II acts as a potent vasoconstrictor and a dipsogenic substance (directly stimulating thirst).
Fluid excretion system:
- ANP (atrial natriuretic peptide, atriopeptin): is secreted by right atrial cardiomyocytes in response to their excessive volumetric stretch.
- Effects of ANP: dilates blood vessels (vasodilation), sharply decreases the secretion of renin, aldosterone, and ADH. As a result, renal reabsorption drops and the excretion of $Na^+$ and water increases, leading to a decrease in CBV.
Briefly: answers to topical questions
What specific stimuli trigger renin secretion by the juxtaglomerular apparatus of the kidneys?
Enzyme secretion by the juxtaglomerular apparatus is regulated by hemodynamic changes, ion concentrations, and the sympathetic nervous system. The main stimuli include:
- Pressure drop — a drop in blood pressure in the afferent arteriole (insufficient blood supply) activates the release of the enzyme.
- Sodium concentration — an increase in the ion concentration in the distal tubule fluid is detected by macula densa cells (macula densa) and enhances secretion.
- Sympathetic influences — direct stimulation via $\beta_1$-adrenergic receptors and the action of adrenaline stimulate the process.
Atrial natriuretic peptide, conversely, decreases enzyme secretion.
What is the sequence of active substance formation in the renin-angiotensin-aldosterone system cascade?
The formation of active substances occurs as a result of sequential enzymatic reactions involving the liver, kidneys, and lungs. The process includes the following stages:
- Angiotensinogen — a substrate protein synthesized by the liver, released into blood plasma, and is inactive.
- Angiotensin I — formed as a result of the action of the renal enzyme renin on angiotensinogen; it is a weakly active decapeptide.
- Angiotensin II — synthesized in the pulmonary circulation under the action of converting enzyme (angiotensin-converting enzyme), which cleaves a fragment from the precursor.
- Aldosterone — its secretion by the adrenal cortex is enhanced under the influence of the formed active angiotensin II.
What mechanisms provide transcapillary fluid exchange according to Starling's law?
Transcapillary fluid exchange between blood and tissues is determined by the difference in hydrostatic and oncotic pressures between blood and interstitial fluid. Sources indicate the following factors:
- Hydrostatic and oncotic pressure of blood and interstitium — their ratio determines transcapillary exchange.
- Plasma oncotic pressure — its decrease leads to fluid transport down the gradient from the vascular bed into the intercellular space.
- Permeability of microvessel walls / capillary membranes — increased permeability facilitates fluid filtration.
- Lymphatic drainage — in chronic lymphostasis, the outflow of intercellular fluid into lymphatic vessels is inhibited.
Additional factors: electrolyte composition, blood pH, and the degree of permeability of capillary membranes.
To remember the order in which vascular mechanisms activate when CBV drops, remember the rule: "Reservoirs react first, pipes second." Veins contract first (venoconstriction, since they hold 60% of the blood), and only after that do arteries narrow.
Class and exam questions
Why might you experience mild dizziness when standing up abruptly?
This is the effect of orthostasis. Upon transitioning to a vertical position, part of the blood is briefly pooled in the veins of the lower extremities and abdominal cavity due to gravity. CBV temporarily drops, reducing blood flow to the brain until baroreceptors are activated.
Which hormone directly triggers the sensation of thirst?
Angiotensin II, formed as part of RAAS activation. It is a dipsogenic substance — it acts on the hypothalamus and triggers the behavioral response of seeking and consuming water (thirst).
Why does the heart secrete hormones (ANP)?
Atrial natriuretic peptide (ANP) protects the heart from volume overload. When circulating blood volume is excessive, the walls of the right atrium stretch, releasing ANP, which suppresses the renin-angiotensin-aldosterone system (RAAS) and prompts the kidneys to actively excrete excess water and sodium.
What else to study on this topic
- Topography and mechanisms of action of baroreceptors in the aortic and sinocarotid zones.
- Detailed physiology of transcapillary exchange: hydrostatic and oncotic pressure.
- Biochemical cascade of the renin-angiotensin-aldosterone system (RAAS).
- Interrelation of functional systems maintaining circulating blood volume, blood pressure, and blood pH.
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