Regulation of Blood Pressure
Arterial blood pressure (BP) is proportionate to the product of the blood flow (cardiac output, CO) and the resistance to passage of blood through precapillary arterioles (peripheral vascular resistance, PVR):
BP = CO × PVR
The rhythmic contraction of the left ventricle, ejecting blood into the vascular system, results in pulsatile arterial pressures.
The peak pressure generated during systolic contraction approximates the systolic arterial blood pressure (SBP);
the lowest arterial pressure during diastolic relaxation is the diastolic blood pressure (DBP).
Pulse pressure is the difference between the systolic and diastolic pressures.
The time-weighted average of arterial pressures during a pulse cycle is the mean arterial pressure (MAP). MAP can be estimated by application of the following formula:
Mean Arterial Pressure
The mean arterial pressure (MAP) is determined by how much blood the heart pumps into the arterial system in a given time (the cardiac output [CO]) and how much resistance the arteries have to this input (total peripheral resistance [TPR]). Mathematically, this is expressed as MAP = CO × TPR. Consequently, all drugs that lower blood pressure work by affecting either the CO or TPR (or both).
The primary determinant of systolic blood pressure (SBP) is CO, whereas the primary determinant of diastolic blood pressure (DBP) is TPR.
Because approximately one third of the cardiac cycle is spent in systole and two thirds in diastole, the MAP can be calculated as MAP = 1/3 SBP + 2/3 DBP.
Blood pressure regulation involves several systems in the body working together.
This is managed by the nervous system to respond quickly to changes in blood pressure.
Baroreceptor Reflex:
- Baroreceptors in the carotid sinus and aortic arch sense changes in blood pressure.
- When blood pressure is high, they send signals to the medulla oblongata, which:
- Decreases heart rate (via parasympathetic stimulation).
- Dilates blood vessels (reduces vascular resistance).
- When blood pressure is low, the brain:
- Increases heart rate and contractility (via sympathetic stimulation).
- Constricts blood vessels (raises vascular resistance).
The carotid sinus baroreceptors send their information to the brainstem using the glossopharyngeal nerve (cranial nerve [CN] IX), whereas the aortic arch baroreceptors use the vagus nerve (CN X) as their afferent nerve.
- Increase in blood pressure causes more stretch on the pressure sensors This causes the baroreceptors to enact changes that will decrease blood pressure. The increased stretch leads to increased firing of the baroreceptors which (1) increase parasympathetic tone through the vagus nerve (CN X) on the SA node to decrease heart rate, and also (2) decrease sympathetic tone.
Decrease in blood pressure causes less stretch on the pressure sensors The decreased stretch causes decreased firing of the baroreceptors; this in turn causes (1) decreased vagal tone to the SA node, resulting in an increased heart rate; as well as (2) increased sympathetic tone to increase heart rate, contractility, and vasoconstriction..
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Carotid sinus massage puts pressure on the baroreceptors in the carotid body, leading to the body “thinking” there is high blood pressure, causing increased parasympathetic tone (as well as decreased sympathetic tone) and therefore a decrease in heart rate. This was previously proposed as a treatment for supraventricular tachycardia (SVT), but is falling out of favor, owing to risk for inducing embolic stroke by massaging cholesterol-laden carotid arteries.
Baroreceptor pathway. The carotid sinus sends its signals via the glossopharyngeal nerve (CN IX), whereas the aortic arch sends its signals via the vagus nerve (CN X) to the brainstem. In both cases, this signal is sent via the nucleus tractus solitarius, which distributes the signal to the body to effect changes in blood pressure.
(From Costanzo LS. Physiology . 4th ed. New York: Elsevier; 2009.)
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Chemoreceptor Reflex:
- Chemoreceptors in the carotid and aortic bodies detect changes in oxygen, carbon dioxide, and pH levels, indirectly affecting blood pressure.
2. Intermediate Regulation (Minutes to Hours)
This involves the hormonal system and vascular adjustments.
Renin-Angiotensin-Aldosterone System (RAAS):
- Low blood pressure or reduced kidney perfusion triggers the release of renin from the kidneys.
- Renin converts angiotensinogen (from the liver) into angiotensin I, which is converted into angiotensin II by the enzyme ACE (mainly in the lungs).
- Angiotensin II:
- Causes vasoconstriction (increases resistance).
- Stimulates the release of aldosterone from the adrenal glands, promoting sodium and water retention by the kidneys (increasing blood volume).
Vasopressin (Antidiuretic Hormone, ADH):
- Released by the posterior pituitary in response to low blood pressure or high plasma osmolarity.
- Promotes water reabsorption in the kidneys, increasing blood volume and pressure.
3. Long-Term Regulation (Hours to Days)
This relies on the kidneys to control blood volume.
Pressure Natriuresis and Diuresis:
- Increased blood pressure increases filtration in the kidneys, leading to:
- Increased sodium and water excretion.
- This reduces blood volume and pressure.
Atrial Natriuretic Peptide (ANP):
- Released by the atria in response to high blood pressure or volume.
- Promotes sodium and water excretion and relaxes blood vessels to lower blood pressure.
4. Additional Factors
- Behavioral and lifestyle adjustments: Exercise, hydration, and stress management can influence blood pressure over time.
- External influences: Medications like ACE inhibitors or beta-blockers are often used to manage dysregulated blood pressure.
By working together, these systems ensure blood pressure remains within a range that supports vital organ function.
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Baroreflexes, mediated by autonomic nerves, act in combination with humoral mechanisms, including the renin-angiotensin-aldosterone system, to coordinate function at these four control sites and to maintain normal blood pressure.
arterioles
postcapillary venules (capacitance vessels)
kidney by regulating the volume of intravascular fluid.
Renin-angiotensin-aldosterone axis
The renin-angiotensin-aldosterone axis is explained in detail in Chapter 9 , but briefly, the juxtaglomerular (JG) cells of the kidney also sense blood pressure. Any decrease in blood flow to the kidney will cause the JG cells to secrete the enzyme renin into the bloodstream. The bloodstream always has angiotensinogen in it, and renin cleaves this angiotensinogen into angiotensin I. Angiotensin I gets cleaved into angiotensin II by angiotensin-converting enzyme (ACE) , which an ACE inhibitor blocks. Angiotensin II is a potent vasoconstrictor , increasing SVR and therefore blood pressure, and also mediates aldosterone release from the zona glomerulosa of the adrenal gland. Aldosterone increases sodium reuptake from the kidney, leading to an expansion in blood volume and thus an increase in blood pressure.
Finally, local release of vasoactive substances from vascular endothelium may also be involved in the regulation of vascular resistance. For example, endothelin-1 constricts and nitric oxide dilates blood vessels.
Reference
Sandeep Chopra, Chris Baby, and Jubbin Jagan Jacob1Neuro-endocrine regulation of blood pressure Indian J Endocrinol Metab. 2011 Oct; 15(Suppl4): S281–S288.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3230096/