In watter siektetoestande is angiotensinogeenvlakke verhoog?  Wat is die implikasies hiervan?

Increased levels of angiotensinogen are associated with Hypertension. High levels of angiotensinogen in the plasma can lead to elevated blood pressure and the body will retain too much fluid. This can also cause the heart to work harder and to grow, can result in heart failure. The synthesis of angiotensinogen is increased by estrogens, thyroid hormones, corticosteroids, ANG II and it is also elevated during pregnancy or when taking estrogen contraceptives.

 

Wat is die rede daarvoor dat middels wat die angiotensienstelsel deur werking op angiotensienreseptore rem, minder newe-effekte het as die wat AOE rem?

Angiotensin receptor blockers are similar to ACE inhibitors, but they have a lower incidence of cough. The blocking of the angiotensin I receptors, the metabolism of Bradykinin to inactive metabolites is not affected which result in the lower incident of dry cough.

 

Op watter wyse het AOE-remmers ‘n tweevoudige meganisme van werking by die behandeling van hipertensie?

ACE inhibitors inhibit the conversion of ANG I to ANG II which is useful in the treatment of hypertension and it also inhibits the degradation of other substances like bradykinin, substance P and enkephalins. This helps with vasodilatation and decreases peripheral resistance and therefore lowers the blood pressure.

 

Op watter tipe angiotensienreseptore werk losartan en soortgelyke middels?  Het hulle enige effekte, direk of indirek, op ander angiotensien II-reseptore?

Losartan and Valsartan are specific competitive antagonists at the AT1 receptors. These drugs are AT1 selective and prolonged treatment will result in the disinhibit of renin release which leads to an increase in the circulating ANG II levels. There might be an increased stimulation of the AT2 receptors which have a indirect effect on AT2 receptors.

 

Wat is die fisiologiese effekte van kiniene op arterieë en vene?  Speel ander outakoïede ‘n rol in hierdie werking?  Verduidelik.

Kinins are known as potent vasodilator peptides. The vasodilatation may be mediated by the release release of NO or vasodilator prostaglandins like PGE2 and PGI2. Other effects of bradykinin include increased release of cAMP, IP3, DAG and also increased capillary permeabilty. All of these contribute to the vasodilatory effects of kinins.

 

Watter reseptor is waarskynlik die mees betrokke in die klinies-belangrike effekte van kiniene?

Bradykinin 2 receptors (B2 receptor)

 

Op watter wyse is natriuretiese peptiede moontlik effektief in die behandeling van hipertensie, asook kongestiewe hartversaking?

The effects of ANP and BNP include vasodilatation, increased Na excretion and GFR, decreased renin secretion, aldosterone mechanism (less Na reabsorption) and inhibits angiotensin II. Because of the vasodilatation and natriuresis, these peptides have been investigated for the treatment of congestive heart failure.

 

Wat is neprilisien en wat is die rasionaal om sy aktiwiteit te inhibeer by die behandeling van hartversaking. Kan jy die middel noem wat sodanig gebruik word. Verwys ook na leereenheid 1 waar julle ook met die spesifieke middel te doen gekry het.

Neprilysin is a neutral endopeptidase (enzyme) that metabolizes ANP and BNP. When this enzyme is inhibited, it results in increased levels of circulating ANP and BNP which leads to increased natriuresis, diuresis and vasodilatation as well as a compensatory increase in renin secretion and plasma ANG II. Due to the increased levels of ANG II, these drugs are not effective as monotherapy in the treatment of heart failure, but in combination with ACE inhibitors. The drug that is used to inhibit neprilysin is Sacubitril.

 

Gee voorbeelde van endotelium-afgeleide vasodilatore en vasokonstriktore.

Vasodilators: CGRP, VIP, Substance P

Vasoconstrictors: NPY