Entries Tagged 'Renin' ↓
October 1st, 2011 — Renin
Renin angiotensin aldosteron system.
Angiotensinogen (x2 globuten from liver)
↓
Angiotensin1
↓ (Bradykin)
↓
Inactive peptide
Angiotensin2
↓ Binds with At1
———————————————————————————
↓ ↓ ↓
↓Blood vessel Adrenal gland ↓sympathetic nervous
↓Cuase vasoconstriction ↓ ↓catecholamine
↓TPR Aldosteron secretion ↓HR
↓BP ↓ ↓cardiac output
Na+,CT reabsorption ↓BP
↓
Blood volume
↓
Cardiac output
↓
BP
TPR= Total peripheral resistance
ACE= Angiotensin converting enzyme
BP= Blood pressure.
- D-2- Methylsucinyl –L- proline had effect similar to SQ20881 but was still only 1/300 as potent the D-isomer, rather than the L-isomer normally sun for amino acid was necessary because of this the isoteric replacement of because NH2 with a CH2 present in suecinyl –L- proline.
- A comparison of the R2 group of the substrate with the methyl groups of D-2-methyl succinyl –L- proline, illustrate that this methyl group occupies same binding site as the side chain of an L-amino.
- One of the most important alterations to succinyl-L-proline was the replacement of the succinyl canboxylate with other groups having enhanced affinity for the atom bound to Ace.
- It produced 3-mercaptopropanoyl-L-proline. This compound has an Ic50 value of 200nm and is more than 1000 times as potent than succinyl-L- proline.
- Addition of a 2-D-methyl group further enhanced is a competitive inhibitors of Ace with a K1 value of 1.7 nm and was the first ACE inhibitor to be marketed.
- Systolic dysfunction can be caused by dilated cardiomyopathes, a reduction in muscle mass.
- Diastolic dysfunction can be cause by increase ventricular stiffness, pericardial disease.
- Both ventricular hypertrophy and myocardial ischemia can contribute to increased ventricular stiffness.
September 30th, 2011 — Medical Science, Renin
Role Of The Renin-Angiotensin Pathway in Cardiovascular disorder.
- The renin-angiotensin pathway is control to the maintenance of blood volume arterial blood pressure and electrolyte balance.
- Excessive release of renin , overproduction of angiotensin2 can contribute to variety of cardiovascular disorder. Specifically over activity of this pathway can result in hypertension on or congestive heart failure (CHF)
- Abnormally high levels of angiotensin2 can contribute to hypertension through both rapid and show pressure response.
- High level of angiotensin2 can caux cellular hypertrophy as increase both tension. All of these events can cause or exacerbate CHF.
- The disease results from conditions in which the heart is unable to supply blood at rate sufficient to meet the demands of the body.
- Similar to hypertension , this pathway physiologic state can occur via a variety of mechanism.
- Any pathophysiologic event which cause either systolie or diastolic dysfunction with result in CHF
Neurogenic signals
↓
Hemodynamic signal ↔ Renin Release ↔ Hormaonal signals
↓
Increased penipheral ↔ Angiotensin2 formation ↔ hypentrophy and remodeling
↓
Regulation or renal function
↓
Slow pressure Response.
September 30th, 2011 — Medical Science, Renin
Angiotensin converting Enzyme inhibitors:
The Renin-Angiotensin Pathway : The renin angiotensin system is a complex highly regulated pathway that is integral in the regulation of blood volume. It consists two main enzymes renin and angiotension converting enzyme whose primary purpose is to release angiotensin2 . Angiotensin2 is a potent vasoconstriction .
Asp-Arg-Val-Tyr-His-Pro-Phe-His-lev-Val-He-R
Angiotensinogen Renin
↓
Asp-Arg-Val-Tyr-His-Pro-Phe-lev, angiotensin1
↓ (angiotesin2, converting, enzyme)
Asp-Arg-Val-Tyr-iie-his-pro-phe, angiotensin
↓ (Aminopeptidase)
Arg-Val-Tyr-lle-his-Pro-Phe,
↓(angiotensin3, endo-and, exopeptidase)
Inactive peptidase
Asp-Arg-Val-Tyr-lle-his-pro
Angiotensin1-7
Fig: Schematic representation of the renin-angiotensin pathway. The lahile peptide bonds of angiotensingen and angiotensin1 are high lighted.
September 30th, 2011 — Medical Science, Renin
Factors involves in Renin Release:
Rennin release is controlled very closely by
– Hemodynamic signals
- Neurogenic signals
- Hormonal signals
-Hemodynamic signals involves the renal juxtaglomerular cell.
-these cell are sensitive to the hemodynamic stretch of the afferent glomerular antenirle .An increased in the stretch implies a raised blood pressure and results in a reduced release of rennin, while a decrease in the stretch increase rennin secretion.
- these cell are also sensitive to Nacl fuse across the macula densa inhibit rennin release , while decrease in the flux stimulate release.
-Neurogenic enhancement of rennin release occurn via activation of B1- receptors.
- finally , a variety of hormonal signals influence the release or renin. Somatostatin atrial natriuretic factor and angiotensin 2 inhibit renin release , whilevasoactive intestinal poptide. Parathyroid hormone.