3.4 - Maintaining Blood Pressure

Tissue Perfusion (Homeostasis Context)

Blood flow through the capillaries and into the body's tissues to supply nutrients and remove waste; ensured by neural, endocrine, renal, and autoregulatory mechanisms

Short-Term Homeostatic Mechanisms

Act quickly to influence peripheral resistance via vasoconstriction/vasodilation or to increase cardiac output

Long-Term Homeostatic Mechanisms

Act more slowly to alter blood volume in order to affect blood pressure

Cardiovascular Centers

Located in the medulla oblongata; regulate blood pressure and flow by responding to changes in blood pressure and blood concentrations of oxygen, carbon dioxide, and hydrogen ions; contain three paired components

Cardioacceleratory Centers

Stimulate cardiac function by increasing heart rate and stroke volume via sympathetic stimulation from the cardiac accelerator nerve

Cardioinhibitory Centers

Slow cardiac function by decreasing heart rate and stroke volume via parasympathetic stimulation from the vagus nerve

Vasomotor Centers

Control vessel tone/contraction of smooth muscle in the tunica media, affecting peripheral resistance, pressure, and flow, mostly via release of norepinephrine from sympathetic neurons

Arteriole Constriction/Dilation Range

Arterioles are normally partially constricted; maximal stimulation can reduce radius to one-half resting state, while full dilation (requiring suppressed sympathetic stimulation) can expand an arteriole by as much as 150 percent

Baroreceptors

Specialized stretch receptors located within thin areas of blood vessels that respond to the degree of stretch caused by blood, sending impulses to the cardiovascular center to regulate blood pressure

Location of Vascular Baroreceptors

Found primarily in sinuses within the aorta (aortic sinuses, in the walls of the ascending aorta just superior to the aortic valve) and the carotid arteries (carotid sinuses, at the base of the internal carotid arteries)

Baroreceptor Reflex - High Blood Pressure

Increased stretch raises baroreceptor firing, stimulating the cardioinhibitory center and inhibiting the cardioacceleratory and vasomotor centers, causing decreased cardiac output, vasodilation, and reduced blood pressure

Baroreceptor Reflex - Low Blood Pressure

Decreased stretch lowers baroreceptor firing, inhibiting the cardioinhibitory center and stimulating the cardioacceleratory and vasomotor centers, causing increased cardiac output and vasoconstriction, raising blood pressure

Chemoreceptors (Blood Pressure Regulation)

Monitor levels of oxygen, carbon dioxide, and hydrogen ions (pH); found near the baroreceptors in the aortic and carotid sinuses; signal both the cardiovascular center and respiratory centers in the medulla oblongata

Chemoreceptor Response to Rising CO2/H+ (Falling pH)

Stimulates the cardioaccelerator and vasomotor centers (increasing cardiac output and constricting peripheral vessels) while suppressing the cardioinhibitory centers; also stimulates respiratory centers to increase respiratory rate

Chemoreceptor Response to Falling CO2/H+ (Rising pH)

Stimulates the cardioinhibitory centers while suppressing the cardioaccelerator and vasomotor centers, decreasing cardiac output and causing peripheral vasodilation

Neuroendocrine Hormones

Hormones such as epinephrine and norepinephrine, produced by neuroendocrine cells in the adrenal medulla, which function both as neurons and endocrine cells; released into the bloodstream in response to neural signals

Epinephrine and Norepinephrine (E and NE) Effects

Enhance and extend the sympathetic "fight-or-flight" response; increase heart rate and force of contraction (raising cardiac output); temporarily constrict vessels to nonessential organs (e.g., digestive tract) while dilating vessels to critical areas (liver, muscles, brain, heart); stimulate liver glucose release

Direct Renal Regulation of Blood Pressure

A non-hormonal mechanism in which increased blood pressure raises glomerular filtration rate (GFR), increasing fluid excretion as urine and decreasing blood volume; decreased blood pressure lowers GFR, promoting water retention and raising blood pressure back to normal

Glomerular Filtration Rate (GFR)

The rate at which the kidneys filter blood

Renin

An enzyme released by juxtaglomerular (JG) cells in the kidneys in response to decreased blood pressure; converts angiotensinogen into angiotensin I

Angiotensinogen

A plasma protein produced by the liver that is converted by renin into angiotensin I

Angiotensin-Converting Enzyme (ACE)

The enzyme, active in the lungs, that converts angiotensin I into angiotensin II

Angiotensin II

A powerful vasoconstrictor that greatly increases blood pressure; stimulates release of ADH and aldosterone, and stimulates the hypothalamic thirst center

ADH (in RAAS Context)

Released from the posterior pituitary in response to angiotensin II; acts on the kidney to increase water reabsorption, increasing blood volume and pressure

Aldosterone

Produced by the adrenal cortex in response to angiotensin II; increases sodium reabsorption by the kidneys, which (since water follows sodium) also increases water reabsorption, raising blood volume and pressure

Renin-Angiotensin-Aldosterone System (RAAS)

The long-term hormonal cascade beginning with renin release that ultimately raises blood volume and blood pressure through angiotensin II, ADH, and aldosterone actions

Erythropoietin (EPO)

A hormone released by the kidneys when blood flow and/or oxygen levels decrease; stimulates erythrocyte production in the bone marrow and acts as a vasoconstrictor

Effects of EPO Overproduction

Overproduction of EPO (or excessive synthetic EPO intake, e.g., for athletic performance enhancement) increases viscosity, resistance, and pressure while decreasing flow, in addition to its vasoconstrictor effect

Atrial Natriuretic Peptide (ANP)

A hormone secreted by cells in the atria of the heart when blood volume is high enough to cause extreme stretching of cardiac cells

B-type Natriuretic Peptide (BNP)

A hormone with effects similar to ANP, produced by cells in the ventricles

Natriuretic Hormone Actions (ANP/BNP)

Act as antagonists to angiotensin II; promote loss of sodium and water from the kidneys, suppress renin, aldosterone, and ADH production/release, promote peripheral vasodilation, and reduce thirst — decreasing blood volume and pressure

Autoregulation Mechanisms

Local, self-regulatory mechanisms requiring neither specialized nervous stimulation nor endocrine control, allowing each tissue region to adjust its own blood flow and tissue perfusion based on local demands; include chemical signals and myogenic controls

Chemical Signals in Autoregulation - Vasodilation Triggers

Decreased oxygen, increased carbon dioxide, elevated lactic acid, potassium or hydrogen ions, inflammatory chemicals, and heightened body temperature open precapillary sphincters, release nitric oxide (a potent vasodilator), and increase tissue perfusion

Chemical Signals in Autoregulation - Vasoconstriction Triggers

Opposite conditions (e.g., adequate oxygen, low carbon dioxide) trigger sphincter constriction and release of endothelins, inducing vasoconstriction

Endothelins (Autoregulation Context)

A family of vasoconstrictor peptides produced by endothelial cells lining blood vessels, playing a crucial role in regulating vessel tone and blood flow by inducing vasoconstriction

Myogenic Response

An autoregulatory mechanism responding to changes in blood flow through arterioles; protects against drastic blood pressure fluctuations by relaxing smooth muscle (dilation, increased flow) when perfusion is low, and contracting smooth muscle (vasoconstriction, decreased flow) when perfusion is excessive

Purpose of the Myogenic Response

Stabilizes blood flow in the capillary network, ensuring adequate oxygen supply without compromising vessel integrity, and prevents ischemia or organ damage from inadequate or excessive blood flow