Long Term Regulation of Blood Pressure

Long term regulation of blood pressure is achieved by RAAS system.

• By changing the blood volume
• By retention of the fluid
• By conservation of the fluid
• By excretion of the fluid

Long term regulation of blood pressure is regulated by blood volume. When blood volume increases blood pressure decreases and when blood volume decreases blood pressure increases.

Blood volume usually regulated by kidneys.

Kidneys have juxta glomerular apparatus. Juxta means next to or close to glomerulus, which contain certain specialized cells which are sensitive to blood flow,  blood pressure and sodium concentration.

Whenever there is loss of blood from body for example dehydration or certain injuries,  haemorrhage. Blood flow or blood volume is decreased which is sense by juxta glomerular apparatus which cause the production of renin.

Renin enters the circulation.  Angiotensiogen secreted and produce by the liver. Renin combine with angiotensiogen in the circulation. By the action of renin angiotensiogen is converted into Angiotensin-I .

Lungs produce the enzyme angiotensin converting enzyme which convert the Angiotensin-I into Angiotensin-II . Angiotensin-II is powerful vasoconstrictor. Which causes the vasoconstriction and the blood pressure is increased.

How Angiotensin-II increase blood pressure by activating sympathetic nervous system?

Angiotensin-II activate the sympathetic nervous system and release epinephrine and norepinephrine.  Which is positively coupled with adenylate cyclase thus increasing cAMP cause the release of calcium ions and thus increases contractility , stroke volume,  heart rate , cardiac output and blood pressure.

How Angiotensin-II increase the blood pressure by acting on adrenal cortex?

Angiotensin-II act on adrenal gland and cause the production of aldosterone.  Which cause the sodium and water retention, reabsorption of sodium in distal convoluted tubule also with water thus increasing the blood volume,  venous return,  cardiac output and blood pressure.

How Angiotensin-II increase blood pressure by acting on posterior pituitary gland?

Angiotensin-II releases anti diuretic hormone (ADH) from posterior pituitary gland which increases the water pores in distal convoluted tubule and connecting tubules, water channels and thus increasing passive absorption of water.

Water retention increases,  diuresis and urination decreases cause retention of blood volume. Thus increasing venous return,  stroke volume , cardiac output and blood pressure.

How blood pressure is increased in dehydration?

Whenever there is dehydration thirst will increased.  We uptake fluid and blood volume is increased.

In thirst hypothalamus is activated which send signal to posterior pituitary gland which increases anti diuretic hormone (ADH) . Then there will be no urination and retention of water thus blood volume will be increased. When the blood volume is increased blood pressure also increases.

Binding of Angiotensin-II to AT1R (Angiotensin-II receptor type 1)

Location of AT1R:

• Arteries
• Kidneys
• Heart
• Adrenal cortex
• Lungs
• Circumventricular organs
• Brain
• Ganglia brain stem

Mechanism of AT1R:

AT1R is activated by vasoconstriction of peptide called Angiotensin-II.  The activated receptor in turns couple to G9/11 and Gi/o which activate phospholipase C and increase cytosolic calcium concentration which increases the stimulation of PKC which is responsible for constriction. Also inhibit the adenylate cyclase and activates various kinases.

Effects of activated AT1R:

• Vasoconstriction which increases blood pressure.
• Aldosterone synthesis and release.
• Increase secretion of anti diuretic hormone.
• Cause cardiac hypertrophy which increse the risk of death.
• Augmentation of peripheral noradrenergic activities.
• Vascular smooth muscle proliferation.
• Decease renal flow increase renin release.
• Renal renin inhibition.
• Renal tubular sodium re uptake which increase blood volume and blood pressure.
• Modulation of central sympathetic nervous system which increase blood pressure.
• Cardiac contractility and increase blood pressure.
• Renal osmocontral and increase electrolytic concentration in blood and increase blood pressure.
• Inflammatory which damage blood vessels and myocardium.
• Hyperlipidaemic which increases risk of cardiac diseases.
• Increase cardiac remodelling (progression of damage).
• Renal damage due to decreased blood flow.
• Increase thirst which increases blood volume and blood pressure.
• Platelet aggregation.

How activated AT1R cause vasoconstriction?

Vasoconstriction:

Vasoconstriction decrease the diameter and increase the total peripheral resistance and blood pressure.

Vasoconstriction can cause damage to endothelium the there will be no epinephrine , PGE2 production and no vasodilation.

Throughout the body Angiotensin-II is the potent vasoconstrictor of arterioles. In kidney angiotensin constricts glomerular arterioles which have greater effect on efferent arterioles than afferent.

How activated AT1R do osmo control?

Osmo control:

Angiotensin-II decreases medullary blood flow through vasa recta which decrease the washout of sodium chloride and urea in the kidney medullary spaces which increase the concentration of sodium chloride and urea which facilitates absorption of tubular fluid.

Angiotensin-II stimulates NA+/H+ exchangers located on the apical membrane (faces of the tubular lumen) which increases sodium reabsorption.

Angiotensin-II increase hypertrophy of renal tubules cells cause further sodium ion reabsorption.

How AT1R release Aldosterone?

Aldosterone release:

Angiotensin-II releases Aldosterone from adrenal cortex (zona glomerolusa). Aldosterone acts on distal convoluted tubule and cortical collecting duct of kidney , reabsorbed sodium ion and water from urine. Thus increasing blood volume and blood pressure.

Basically Aldosterone stimulates the genes which codes for NA+/K+ antiport channel.

How AT1R release anti diuretic hormone (ADH)?

Release of ADH / vassopression:

Angiotensin-II releases ADH from posterior pituitary gland. ADH made in hypothalamus and stored and released from posterior pituitary gland when stimulated by Angiotensin-II.

As name suggests it is a vasoconstriction but main function is to reabsorb water from urine in kidneys.

It also acts on central nervous system

Increase appetite for salt

Increase thirst

Both increases the blood pressure.

How AT1R act as hyperlipidaemic?

Hyperlipidaemic:

It stimulates some proteins which attaches to the surface of vessels to make an atherosclerotic plaque. The important targeted function of RAAS is vasoconstriction and aldosterone release.

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