SYSTEMIC MECHANISM OF BLOOD PRESSURE CONTROL

  • 03 Pages
  • Published On: 17-11-2023

INTRODUCTION

Blood pressure refers to the force which blood pumped from the heart flows in the peripheral blood vessels. The optimal systolic blood pressure ranges between 90 – 120 mmHg while the optimal diastolic blood pressure ranges between 60 – 80 mmHg. Primarily, an individual’s blood pressure depends on the volume of blood in circulation, blood viscosity, cardiac output, elasticity of the blood vessel walls and the peripheral vascular resistance (Jennifer L. et. al., 2016).

Endogenous and exogenous chemical substances can also contribute to the blood pressure. Angiotensin (11) and Glyceryl trinitrate (nitroglycerin) increase and decrease blood pressure when administered to a patient. Angiotensin (11) is used for its vasopressor action in patients with low blood pressure due to circulatory shock (Lawrence W. et. al., 2017).

Angiotensin (11) increases blood pressure by constricting the blood vessels, increasing sympathetic nerve stimulation where noradrenaline is released and acts on the cardiovascular system to increase cardiac output (Jess Speller , 2020).

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RESULTS

The basal arteriole blood pressure is 125/75 mmHg. Administration of Angiotensin (11) results in a gradual rise in the systolic and diastolic blood pressure. The systolic blood pressure rises by 28 % while the diastolic blood pressure rises by 60%. Blood pressure remains constant but begins to decrease once the effect of Angiotensin 11 reduces. Administration of Glyceryl trinitrate causes a drop in blood pressure. Systolic blood pressure drops by 31% while the diastolic blood pressure drops by 58%.

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DISCUSSION

Angiotensin (11) is a vasopressor (Khaana A. et al. 2017). It is generated from the RAAS where when Angiotensin 1 is converted to Angiotensin (11) by Angiotensin Converting Enzyme present in lungs endothelium and in the blood vessel walls. Angiotensin (11) acts on the G-protein coupled receptor AT-1 located on the endothelial surface of arterioles. Its binding activates the G-q protein that activates and increases the activity of phospholipase C (PLC). PLC increases the generation rate of the second messengers Inositol triphosphate and Diacylglycerol which increase intracellular sequestration of calcium ions and calcium channels allow more calcium into the cell, facilitating smooth muscle contraction and increases the total peripheral resistance (Jess Speller, 2020). Hence, blood pressure rises steadily from the basal 125/75 mmHg t0 160/120mmHg.

Glyceryl trinitrate is a prodrug that undergoes de-nitration to a nitrite anion which is further reduced to nitric oxide (NO) which is a vasodilator. NO activates guanylyl cyclase that generates cyclin guanosine monophosphate (cGMP) which is the substrate of the cGMP dependent protein kinase (The American Society of Health System Pharmacists, 2016). Dephosphorylation of the myosin light chain occurs, relaxing the smooth muscles, resulting in vasodilation which increases the diameter of the blood vessels enabling blood pressure to fall to below the basal pressure to 110/50mmHg. The heart rate and the heart force remain constant because Angiotensin (11) increases the blood pressure levels without altering the other parameters by resetting the baroreflex control mechanism to adapt to the high pressure through G-protein coupled AT-1 receptors (American Physiological Society, 2016). Additionally, it withdraws the vagal tone, hence the heart rate does not rise.

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REFERENCES
  1. American Physiological Society. Angiotensin 11 and Baroreflex Control of Heart Rate. 2016 Journal.
  2. Drugs.com."Nitro-Dur - FDA prescribing information, side effects and uses". drugs.com. Archived from the original on 1 April 2017. Retrieved 31 March 2017. 2019.
  3. Jennifer L. Lapum, Margaret Verkuyl, Wendy Garcia, Oona St-Amant, and Andy Tan. Vital Sign Measurement across the Lifespan – 1st Canadian Edition. 2016.
  4. Jess Speller. The Renin-Angiotensin-Aldosterone-System. 2020. https://teachmephysiology.com/urinary-system/regulation/the-renin-angiotensin-aldosterone-system/
  5. Khanna A., English S. W., Wang X. S., Ham K., Tumlin J., Szerlip H., Busse L. W., Altaweel L., Albertson T. E., Mackey C., et al. Angiotensin II for the treatment of vasodilatory shock. N Engl J Med. 2017;377(5):419–30.
  6. Lawrence W. Busse et. al. The effect of angiotensin II on blood pressure in patients with circulatory shock: a structured review of the literature. Article number: 324 (2017)
  7. "Nitroglycerin". The American Society of Health-System Pharmacists. Archived from the original on 21 December 2016. Retrieved 8 December 2016.

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