The coice of the type of hypertension depends on your experimental question.In AngII-hypertension you will be dealing with the combined effect of AngII, aldosterone and high blood pressure. In the case of high salt alone, you will not usually induce hypertension, unless you choose  some specific models, such as the Dahl-salt sensitive rat, or you combine high salt with 5/6 nephrectopmy. In the DOCA-salt hypertension, you will induce hypertension along with suppression of the endogenous renin-angiotensin system combined with potasium depletion and generate a state of exogenous mineralocorticoid excess. These models differ considerably in terms of tissue/cellular impact. We need to know, then, what it is that you would like to study.

Which animal model are you using? In the swine model, both DOCA (no salt, no nephrectomy) and Ang-II will induce similar levels of hypertension

Would you please kondly read my review article ,which appeared in Heart Failure Review 2008;13:273-284:

New insights into the importance of aminopeptidase A in hypertension.

Mizutani S1, Ishii M, Hattori A, Nomura S, Numaguchi Y, Tsujimoto M, Kobayshi H, Murohara T, Wright JW.

Author information

1Department of Medical Science of Proteases, Nagoya University, Graduate School of Medicine, Nagoya, Japan.

Abstract

The renin-angiotensin system (RAS) plays an important role in the maintenance of normal blood pressure and the etiology of hypertension; however, minimal attention has been paid to the degradation of the effector peptide, angiotensin II (AngII). Since aminopeptidase A (APA)-deficient mice develop hypertension APA appears to be an essential enzyme in the control of blood pressure via degradation of AngII. The robust hypertension seen in the spontaneously hypertensive rat (SHR) is due to activation of the RAS, and an accompanying decrease in kidney APA. Changes in APA have also been measured during the activation of the RAS in the Goldblatt hypertension model and Dahl salt-sensitive (DSS) rat. The DSS rat shows an elevation in renal APA activity at the onset of hypertension suggesting a protective role against elevations in circulating AngII, followed by decreased APA activity with advancing hypertension. Changes seen in human maternal serum APA activity during preeclampsia are similar to changes measured in renal APA in the DSS rat model. APA activity is higher than during normal pregnancy at the onset of preeclampsia, and with advancing preeclampsia (severe preeclampsia) declines below that seen during normal pregnancy. Serum APA activity is also increased during hormone replacement therapy (HRT), perhaps in reaction to elevated levels of AngII. Thus, it appears important to consider the relationship among activation of the RAS, circulating levels of AngII, and the availability of APA in hypertensive disorders.

PMID:

17990103

[PubMed - indexed for MEDLINE]

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Publication Types, MeSH Terms, Substances

How far Angiotensin II (Ang II) system induced hypertension is similar or different from dietary hypertension?

1) First of all, they are similar in that they all induce high blood pressure (hypertension) through increase of vascular intracellular calcium and increase of the concentration of salt in blood stream (see aldosterone in AngII pathway/system)

2) Secondly, they are different because the mechanism of action of Ang II is different from that of NaCl, at least at the level of the vessels.

a. Angiotensin II (Ang II), a potent vasoactive peptide with mitogenic potential, influences vascular smooth muscle cell contraction and growth through receptor (AT1 or AT2) -linked pathways that increase intracellular free Ca2+ concentration (Touyz , Schiffrin , 1997)

b. NaCl does not bind receptors. The increase of extracellular concentration of Na+ directly causes myocyte depolarisation (by inflow of Na+). The depolarisation induces the opening of voltage dependent Ca2+ Channels and Ca2+ flows in the cells. The peripheral resistances are progressively increased by the augmentation of intracellular concentration of Ca2+ in vascular myocyte (Dimo et al., 1999; Bopda et al., 2007).

From the above mechanisms you may decide on what to  do.  You need to have clear objectives in mind, with regards to your research project

I am looking for a lab that is using BP-1/6C3/aminopeptidase A-deficient mice.

I would like to ask a collaborative study for aminopeptidase A-deficient mice. and I would appreciate it if the lab would contact me.