H1 receptors on smooth muscles

[RB&C]

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I'm confused regarding the different effects of histamine on H1 receptors.

According to Lippincotts, " H1 receptors are important in producing smooth muscle contraction and increasing capillary permeability."

So...the muscle in the arteries contracts to increase permeability? Is that the effect of H1 on arteries? So the arteries should vasocontrict as well, but due to NO release, they dilate. but the contraction of the cells, is that related to muscle?
I'm just not understanding this fully.

Help.

 

[Entadus]

remember there are multiple layers of smooth muscle in an artery... muscularis interna, propria, etc

with one layer being circumferential, when it contracts the artery lumen is narrowed (vasoconstriction, think alpha-1 adrenoceptor)

the other layer has longitudinal muscle fibers, so when it contracts the artery shortens (that is, the gaps between endothelial cells get bigger), increasing permeability. This effect is most apparent in the post-capillary venules during the acute inflammatory response.

Not sure about the exact molecular bio of the Histamine H1 receptor.

EDIT: SDN is not for homework help

 

[RB&C]

Yes, i thought about that. I was wondering if the H1 receptors are on the longitudinal fibers rather than the circumferential? I literally didn't read this anywhere. I didn't want to sound stupid. I'm confused because the bronchial tree smooth muscles contract, but the smooth muscles in the arteries contract in a different way. I looked at Guytons, nothing. It's not a homework question. It's merely curiosity. I'm bad at understanding receptors and their functions. If there are rules as to what questions should be posted, where should i read them?

 

[RB&C]

remember there are multiple layers of smooth muscle in an artery... muscularis interna, propria, etc

with one layer being circumferential, when it contracts the artery lumen is narrowed (vasoconstriction, think alpha-1 adrenoceptor)

the other layer has longitudinal muscle fibers, so when it contracts the artery shortens (that is, the gaps between endothelial cells get bigger), increasing permeability. This effect is most apparent in the post-capillary venules during the acute inflammatory response.

Not sure about the exact molecular bio of the Histamine H1 receptor.

EDIT: SDN is not for homework help

Yes, i thought about that. I was wondering if the H1 receptors are on the longitudinal fibers rather than the circumferential? I literally didn't read this anywhere. I didn't want to sound stupid. I'm confused because the bronchial tree smooth muscles contract, but the smooth muscles in the arteries contract in a different way. I looked at Guytons, nothing. It's not a homework question. It's merely curiosity. I'm bad at understanding receptors and their functions. If there are rules as to what questions should be posted, where should i read them?

 

[iBS1972]

In short: vasodilation (via PLC pathway mediated NO release), and bronchoconstriction (via PLC mediated Ca++ release), among other effects. It does not cause vasoconstriction. This is the classic physiological effect of histamine.

H1 effects
Stimulation of H1 receptors, which are coupled to phospholipase C, induces:

1. Capillary vasodilation and Increased capillary permeability. Vasodilation, resulting from nitric oxide release, can give flushing of the face and headache and tends to lower arterial pressure. In case of anaphylactic shock, there is an important release of histamine, inducing blood trapping in dilated vessels and collapse. Increased capillary permeability is responsible for edema resulting from leakage of protein and fluid from plasma into the extracellular spaces, by opening of precapillary sphincters and capillary dilation enhanced by contraction of efferent veins.
2. Contraction of smooth muscles, in particular bronchial and digestive ones, via G proteins which activate phospholipase C, leading to an increase in intracellular Ca2+. An aerosol of histamine elicits a bronchoconstriction, but the pathophysiological role of histamine in asthma does not seem important.
3. Increase in vigilance by a central effect: inhibition of this stimulant effect by H1-antihistamines, which cross blood-brain barrier, explains their sedating effect.

H2 effects
Stimulation of H2 receptors which act through cyclic AMP induces:

1. increase of gastric secretion of hydrochloric acid, HCl, which can be regarded as the main H2 effect. Stimulation of HCl secretion by histamine involves a cascade of reactions: stimulation of H2 receptors, activation of adenylcyclase, increase in cyclic AMP which modulates the activity of proteins kinases, which themselves activate H+/K+-ATPASE, responsible of excretion of protons in gastric fluid.
2. cardiac stimulation: positive inotropic and chronotropic effects.
3. vasodilation: stimulation of H2 receptors induces vasodilation, but the H2 vasodilatator effect of slower onset and more durable than that of H1.
4. small bronchodilatator effect.
5. possible inhibition of prolactin release.

Histamine - Pharmacorama