Physiology, Arterial Pressure Regulation

Article Author:
James Shahoud
Article Editor:
Narothama Aeddula
Updated:
2/11/2019 11:57:14 AM
PubMed Link:
Physiology, Arterial Pressure Regulation

Introduction

In general, an individual’s “blood pressure,” or systemic arterial pressure, refers to the pressure measured within large arteries in the systemic circulation. This number splits into systolic blood pressure and diastolic blood pressure. Blood pressure is traditionally measured using auscultation with a mercury-tube sphygmomanometer. It is measured in millimeters of mercury and expressed in terms of systolic pressure over diastolic pressure. Systolic pressure refers to the maximum pressure within the large arteries when the heart muscle contracts to propel blood through the body. Diastolic pressure describes the lowest pressure within the large arteries during heart muscle relaxation between beating. 

Arterial pressure directly corresponds to cardiac output, arterial elasticity, and peripheral vascular resistance.  Blood pressure is remarkably easy to alter and can be affected by many activities.  Maintaining blood pressure within normal limits is essential. A blood pressure between 140/80 mmHg to 159/99 mmHg is classified to as stage 1 hypertension. Categorization of Stage 2 hypertension is a pressure between 160/100 mmHg to 179/109 mmHg.[1] Hypertensive urgency describes a blood pressure greater than 180/110 mmHg and hypertensive emergency refers to a very high blood pressure that results in potentially life-threatening symptoms and end-organ damage. Hypotension, on the other hand, is a blood pressure less than 90/60 mmHg. It is crucial for the body to be able to adjust to acute changes in blood pressure and for the patient to receive medical treatment or lifestyle adjustments for chronic variations.

Mechanism

There are several mechanisms through which the body regulates arterial pressure.

Baroreceptor Reflex

In response to acute changes in blood pressure, the body responds through the baroreceptors located within blood vessels. Baroreceptors are a form of mechanoreceptor that become activated by the stretching of the vessel. This sensory information is conveyed to the central nervous system and used to influence peripheral vascular resistance and cardiac output.

There are two forms of baroreceptors.

High-Pressure Baroreceptors

Two baroreceptors are located within the high-pressure arterial system.

  • The carotid baroreceptor responds to both increases and decreases in blood pressure and sends afferent signals via the glossopharyngeal nerve (CN IX).
  • The aortic arch baroreceptor responds only to increases in blood pressure, sending its signals through the vagus nerve (CN X).

These both send signals in response to the physical distortion of the vessel. The stretch of the vessel leads to an increase in action potential relayed from the sensory endings located in the tunica adventitia of the artery. These action potentials get transmitted to the solitary nucleus that signals to autonomic neurons secrete hormones to affect the cardiovascular system. Activation of the aortic baroreceptor during increases in blood pressure effectively inhibits the efferent sympathetic nerve response.[2] On the other hand, if an individual’s blood pressure were to fall such as in hypovolemic shock, the rate of action potential from the baroreceptors would be decreased due to reduced depolarization; this would lead to reduced inhibition of sympathetic activity, resulting in a reflex to increase pressure.

Low-Pressure Baroreceptors

These baroreceptors are present within the low-pressure venous system. They exist within large veins, pulmonary vessels, and within the walls of the right atrium and ventricle. The venous system has compliance approximately 30 times greater than that of the arterial system [3]. Changes in volume largely influence the baroreceptors in the venous system. Decreased frequency in action potentials in low-pressure scenarios leads to the secretion of antidiuretic hormone, renin, and aldosterone. These lead to a downstream effect to regulate arterial pressure.

Antidiuretic Hormone

Antidiuretic hormone (ADH), also known as vasopressin, is a hormone synthesized in the magnocellular neurosecretory cells within the paraventricular nucleus and supraoptic nucleus of the hypothalamus. ADH is synthesized and released in response to multiple triggers which are:

  1. High serum osmolarity, which acts on osmoreceptors in the hypothalamus
  2. Low blood volume causes a decreased stretch in the low-pressure baroreceptors, leading to the production of ADH
  3. Decreased blood pressure causes decreased stretch in the high-pressure baroreceptors, also leading to the production of ADH
  4. Angiotensin II

The antidiuretic hormone produced in the hypothalamus makes its way down the pituitary stalk to the posterior pituitary where it is kept in reserve for release in response to the above-listed triggers. ADH mainly functions to increase free water reabsorption in the collecting duct of the nephrons within the kidney, causing an increase in plasma volume and arterial pressure. ADH in high concentrations has also been shown to cause moderate vasoconstriction, increasing peripheral resistance, and arterial pressure.[4][5]

Renin-Angiotensin-Aldosterone System (RAAS)

The renin-angiotensin-aldosterone system is an essential regulator of arterial blood pressure. The system relies on several hormones that act to increase blood volume and peripheral resistance. It begins with the production and release of renin from juxtaglomerular cells of the kidney. They respond to decreased blood pressure, sympathetic nervous system activity, and reduced sodium levels within the distal convoluted tubules of the nephrons. In response to these triggers, renin is released from the juxtaglomerular cells and enters the blood where it comes in contact with angiotensinogen which is produced continuously by the liver. The angiotensinogen is converted into angiotensin I by renin. The angiotensin I then make its way to the pulmonary vessels, where the endothelium produces the angiotensin-converting enzyme (ACE). Angiotensin I is then converted to angiotensin II by ACE. Angiotensin II has many functions to increase arterial pressure, including:

  • Potent vasoconstriction of arterioles throughout the body
  • Vasoconstriction of the efferent arterioles within the glomerulus of the kidney, resulting in the maintenance of glomerular filtration rate
  • Increased sodium reabsorption within the kidney tubules - the increased sodium reabsorption from the kidney tubules results in passive reabsorption of water through osmosis; this causes an increase in blood volume and arterial pressure
  • The release of antidiuretic hormone (ADH) release from the posterior pituitary gland
  • The release of aldosterone from the zona glomerulosa of the adrenal cortex within the adrenal gland
    • Aldosterone functions to increase the arterial pressure through the upregulation of Na+/K+ pumps of the distal convoluted tubule and collecting duct within the nephron
    • This activity is the distal convoluted tubule leads to increased reabsorption of sodium, as well as increased secretion of potassium
    • The increase in sodium reabsorption leads to passive reabsorption of water and an increase in blood pressure

Clinical Significance

The role of arterial pressure regulation is to maintain a high enough pressure that allows for proper perfusion of body tissue and organs; but not so high as to cause bodily harm. When the body enters a state of acute hypotension, the baroreflex function attempts to return arterial pressure to its stable state to allow continuous perfusion.[6] The body may enter a state of chronic hypertension, but most often there is not an identifiable cause but rather a consequence of the interaction between multiple risk factors. The term for this condition is essential hypertension. It represents approximately 95% of patients with hypertension.[7][8] Treating hypertension is critical because it can result in cerebral, cardiac, and renal complications. First line medications to treat essential hypertension include calcium channel blockers, ACE inhibitors, angiotensin receptor blockers, and thiazide diuretics. 


References

[1] Reboussin DM,Allen NB,Griswold ME,Guallar E,Hong Y,Lackland DT,Miller EPR 3rd,Polonsky T,Thompson-Paul AM,Vupputuri S, Systematic Review for the 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2018 Oct 23     [PubMed PMID: 30354656]
[2] Sanders JS,Mark AL,Ferguson DW, Importance of aortic baroreflex in regulation of sympathetic responses during hypotension. Evidence from direct sympathetic nerve recordings in humans. Circulation. 1989 Jan;     [PubMed PMID: 2910547]
[3] Gelman S, Venous function and central venous pressure: a physiologic story. Anesthesiology. 2008 Apr;     [PubMed PMID: 18362606]
[4] McClure JM,Rossi NF,Chen H,O'Leary DS,Scislo TJ, Vasopressin is a major vasoconstrictor involved in hindlimb vascular responses to stimulation of adenosine A(1) receptors in the nucleus of the solitary tract. American journal of physiology. Heart and circulatory physiology. 2009 Nov;     [PubMed PMID: 19749166]
[5] Henderson KK,Byron KL, Vasopressin-induced vasoconstriction: two concentration-dependent signaling pathways. Journal of applied physiology (Bethesda, Md. : 1985). 2007 Apr;     [PubMed PMID: 17204577]
[6] Zhang R,Behbehani K,Crandall CG,Zuckerman JH,Levine BD, Dynamic regulation of heart rate during acute hypotension: new insight into baroreflex function. American journal of physiology. Heart and circulatory physiology. 2001 Jan     [PubMed PMID: 11123258]
[7] Carretero OA,Oparil S, Essential hypertension. Part I: definition and etiology. Circulation. 2000 Jan 25     [PubMed PMID: 10645931]
[8]     [PubMed PMID: 14597461]