arteriole

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Related to Efferent arteriole: Peritubular capillaries

ar·te·ri·ole

 (är-tîr′ē-ōl′)
n.
One of the small terminal branches of an artery, especially one that connects with a capillary.

[New Latin artēriola, diminutive of Latin artēria, artery, from Greek artēriā; see wer- in Indo-European roots.]

ar·te′ri·o′lar (-ō′lər, -ə-lər) adj.

arteriole

(ɑːˈtɪərɪˌəʊl)
n
(Anatomy) anatomy any of the small subdivisions of an artery that form thin-walled vessels ending in capillaries
[C19: from New Latin arteriola, from Latin artēria artery]

ar•te•ri•ole

(ɑrˈtɪər iˌoʊl)

n.
any of the smallest branches of an artery.
[1830–40; < New Latin artēriola]
ar•te`ri•o′lar, adj.

ar·te·ri·ole

(är-tîr′ē-ōl′)
Any of the smaller branches of an artery, especially one that ends in the capillaries.

arteriole

A small artery supplying blood from a main artery to a capillary.
ThesaurusAntonymsRelated WordsSynonymsLegend:
Noun1.arteriole - one of the small thin-walled arteries that end in capillariesarteriole - one of the small thin-walled arteries that end in capillaries
arteria, arterial blood vessel, artery - a blood vessel that carries blood from the heart to the body
Translations

ar·te·ri·ole

n. arteriola, arteria diminuta que termina en un capilar.
References in periodicals archive ?
The rising systemic blood pressure triggered by renin-angiotensin-aldosterone system could compensate the hemodynamic effects of stenotic lesions, regulation of afferent, and efferent arteriole could temporary maintain the glomerular filtration ability, not every RAS would then lead in renal ischemia and influence the eGFR result.
Despite the increase in renal blood flow, the pressure within the glomerulus remains unaltered owing to compensatory effects on the afferent and efferent arteriole, but this only occurs in a normal kidney.
In the kidney, it causes strong vasoconstriction of the efferent arteriole and moderate vasoconstriction of the afferent arteriole, directly stimulates the reabsorption of sodium ions in the proximal tubule, thereby contributing to an increased volume of extracellular fluid and the development of hypertension [1,2].
Dilation of the afferent arteriole or constriction of the efferent arteriole will increase GFR.
Angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin-receptor blockers (ARBs) decrease renal blood perfusion by inhibiting angiotensin II-mediated vasoconstriction at the efferent arteriole.
The glomerular capillaries are supplied by the afferent arteriole; blood then flows out of the glomerular capillaries via the efferent arteriole.
Renal artery stenosis is a contraindication for ACE-inhibition: where there is impaired flow into the glomerulus, angiotensin II maintains glomerular filtration pressure by constricting the efferent arteriole.
The ensuing increase in angiotensin II production maintains both the intraglomerular pressure and the GFR, increasing the resistance at the efferent arteriole.