Anti-stress & anti-anxiety effects of angiotensin II AT1 receptor antagonists.

[Guest guest]

I'm not sure if anyone has mentioned the recent study below. It

basically says that ARB drugs like Benicar may have significant

effects on the nervous system, which therefore would have an indirect

effect on the immune system (i.e. lowering stress reactions helps to

lower TH2 responses). Thus, IMHO, any discussion on how such ARBs

help people, also have to take such effects into account.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=

Retrieve & db=pubmed & dopt=Abstract & list_uids=15837532 & query_hl=41

Regulatory Peptides

Volume 128, Issue 3 , 30 June 2005, Pages 227-238

Molecular Physiology of Vasoactive

Abstract

The brain and the peripheral (hormonal) angiotensin II systems are

stimulated during stress. Activation of brain angiotensin II AT1

receptors is required for the stress-induced hormone secretion,

including CRH, ACTH, corticoids and vasopressin, and for stimulation

of the central sympathetic activity. Long-term peripheral

administration of the angiotensin II AT1 antagonist candesartan blocks

not only peripheral but also brain AT1 receptors, prevents the

hormonal and sympathoadrenal response to isolation stress and prevents

the formation of stress-induced gastric ulcers. The mechanisms

responsible for the prevention of stress-induced ulcers by the AT1

receptor antagonist include protection from the stress-induced

ischemia and inflammation (neutrophil infiltration and increase in

ICAM-1 and TNF-α) in the gastric mucosa and a partial blockade of

the stress-induced sympathoadrenal stimulation, while the protective

effect of the glucocorticoid release during stress is maintained. AT1

receptor antagonism prevents the stress-induced decrease in cortical

CRH1 and benzodiazepine binding and is anxiolytic.

Conclusions

Recent experiments indicate possible novel therapeutic effects of Ang

II AT1 receptor blockade. AT1 receptor blockade antagonizes the

effects of AT1 receptor stimulation in peripheral organs integrating,

together with hypothalamic structures, the HPA axis, and in higher

brain centers such as the amygdala [99] involved in the processing of

sensory information and the behavioral response to stress (Fig. 12).

In this way, the AT1 receptor antagonist modulates the stress-induced

glucocorticoid feedback in the same structure. Modulation

of the central response to stress, and specific peripheral effects of

AT1 receptor antagonists, decreases the vulnerability and sensitivity

to stress, preventing stress-related disorders.

Besides its established role in treatment of hypertension, a novel

role emerges for the use of peripheral and centrally acting

insurmountable AT1 receptor antagonists as therapeutically

advantageous for the prevention and treatment of ischemic,

inflammatory, anxiety and stress-related disorders.

[Guest guest]

This is absolutely in line with my own experience. My mental stress

decreased tremendously with Benicar. I was more relaxed, didn't get

upset about things so easily, could sleep rather than worrying a

problem to death, and the old teeth chattering stopped (a nervous

kind of thing I couldn't control). Neck tension disappeared, etc.,

etc., etc. This was all in addition to the tremendous pain relief,

migraine relief etc. Benicar is definitely working on more than

Blood pressure in my case, I have no doubt about that. As a matter

of fact, it hasn't affected my bp much at all (unless it's keeping

it as low as it's always been).

penny

> I'm not sure if anyone has mentioned the recent study below. It

> basically says that ARB drugs like Benicar may have significant

> effects on the nervous system, which therefore would have an

indirect

> effect on the immune system (i.e. lowering stress reactions helps

to

> lower TH2 responses). Thus, IMHO, any discussion on how such ARBs

> help people, also have to take such effects into account.

>

> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=

> Retrieve & db=pubmed & dopt=Abstract & list_uids=15837532 & query_hl=41

>

> Regulatory Peptides

> Volume 128, Issue 3 , 30 June 2005, Pages 227-238

> Molecular Physiology of Vasoactive

>

> Abstract

>

> The brain and the peripheral (hormonal) angiotensin II systems are

> stimulated during stress. Activation of brain angiotensin II AT1

> receptors is required for the stress-induced hormone secretion,

> including CRH, ACTH, corticoids and vasopressin, and for

stimulation

> of the central sympathetic activity. Long-term peripheral

> administration of the angiotensin II AT1 antagonist candesartan

blocks

> not only peripheral but also brain AT1 receptors, prevents the

> hormonal and sympathoadrenal response to isolation stress and

prevents

> the formation of stress-induced gastric ulcers. The mechanisms

> responsible for the prevention of stress-induced ulcers by the AT1

> receptor antagonist include protection from the stress-induced

> ischemia and inflammation (neutrophil infiltration and increase in

> ICAM-1 and TNF-α) in the gastric mucosa and a partial blockade of

> the stress-induced sympathoadrenal stimulation, while the

protective

> effect of the glucocorticoid release during stress is maintained.

AT1

> receptor antagonism prevents the stress-induced decrease in

cortical

> CRH1 and benzodiazepine binding and is anxiolytic.

>

> Conclusions

>

> Recent experiments indicate possible novel therapeutic effects of

Ang

> II AT1 receptor blockade. AT1 receptor blockade antagonizes the

> effects of AT1 receptor stimulation in peripheral organs

integrating,

> together with hypothalamic structures, the HPA axis, and in higher

> brain centers such as the amygdala [99] involved in the processing

of

> sensory information and the behavioral response to stress (Fig.

12).

> In this way, the AT1 receptor antagonist modulates the stress-

induced

> glucocorticoid feedback in the same structure. Modulation

> of the central response to stress, and specific peripheral effects

of

> AT1 receptor antagonists, decreases the vulnerability and

sensitivity

> to stress, preventing stress-related disorders.

>

> Besides its established role in treatment of hypertension, a novel

> role emerges for the use of peripheral and centrally acting

> insurmountable AT1 receptor antagonists as therapeutically

> advantageous for the prevention and treatment of ischemic,

> inflammatory, anxiety and stress-related disorders.

[Guest guest]

Hi Mark,

I can't access Medline right now. Were the authors talking about

experiments they did or were they reviewing others' experiments? Do

you know what the experiments were? The part of the abstract you

quoted seemed awfully vague.

>> Recent experiments indicate possible novel therapeutic effects of Ang

>> II AT1 receptor blockade.

Sue ,

Upstate New York