Persistent Agonist-Induced Vasoconstriction Is Not Required for Angiotensin II to Mediate Inward Remodeling of Isolated Arterioles with Myogenic Tone

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Abstract

Norepinephrine (NE, 10–5.5 M) exposure for 4 h induces tone augmentation and vasodilation impairment after its removal. These changes are believed to represent early stages of inward remodeling. The hypothesis was tested that adrenoceptors causing vasoconstriction are responsible for NE-induced maintenance of augmented tone and vasodilation impairment, and that other vasoconstrictors associated with in vivo inward remodeling, a condition in which the internal passive diameter of arterioles is reduced without changes in medial cross-sectional area, also induce these changes in isolated arterioles. α-Adrenoceptor blockade prevented tone augmentation and vasodilation impairment, while β-adrenoceptor blockade allowed NE to induce those changes plus inward remodeling. Endothelin-1 (10–8 M) induced tone augmentation and vasodilation impairment. Angiotensin II (ANG-II, 10–7 M) and platelet-derived growth factor (10 ng/ml) did not. ANG-II did not cause sustained vasoconstriction, but induced inward remodeling dependent on presence of myogenic tone and tyrosine phosphorylation. Thus, prolonged vasoconstriction is not required during ANG-II-induced inward remodeling, suggesting remodeling processes effected by different agonists vary, with tone augmentation and impaired vasodilation occurring when vasoconstriction is required. This stresses the dynamic structure of arterioles, with rapid remodeling possibly involving functional changes and changes in extracellular matrix, cellular attachments, and/or cytoskeletal structures.

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Regulation of arterial diameter and wall [Ca2+] in cerebral arteries of rat by membrane potential and intravascular pressure.

Ken M. Nelson, J. Knot (1998)

1. The regulation of intracellular [Ca2+] in the smooth muscle cells in the wall of small pressurized cerebral arteries (100-200 micron) of rat was studied using simultaneous digital fluorescence video imaging of arterial diameter and wall [Ca2+], combined with microelectrode measurements of arterial membrane potential. 2. Elevation of intravascular pressure (from 10 to 100 mmHg) caused a membrane depolarization from -63 +/- 1 to -36 +/- 2 mV, increased arterial wall [Ca2+] from 119 +/- 10 to 245 +/- 9 nM, and constricted the arteries from 208 +/- 10 micron (fully dilated, Ca2+ free) to 116 +/- 7 micron or by 45 % ('myogenic tone'). 3. Pressure-induced increases in arterial wall [Ca2+] and vasoconstriction were blocked by inhibitors of voltage-dependent Ca2+ channels (diltiazem and nisoldipine) or to the same extent by removal of external Ca2+. 4. At a steady pressure (i.e. under isobaric conditions at 60 mmHg), the membrane potential was stable at -45 +/- 1 mV, intracellular [Ca2+] was 190 +/- 10 nM, and arteries were constricted by 41 % (to 115 +/- 7 micron from 196 +/- 8 micron fully dilated). Under this condition of -45 +/- 5 mV at 60 mmHg, the voltage sensitivity of wall [Ca2+] and diameter were 7.5 nM mV-1 and 7.5 micron mV-1, respectively, resulting in a Ca2+ sensitivity of diameter of 1 mum nM-1. 5. Membrane potential depolarization from -58 to -23 mV caused pressurized arteries (to 60 mmHg) to constrict over their entire working range, i.e. from maximally dilated to constricted. This depolarization was associated with an elevation of arterial wall [Ca2+] from 124 +/- 7 to 347 +/- 12 nM. These increases in arterial wall [Ca2+] and vasoconstriction were blocked by L-type voltage-dependent Ca2+ channel inhibitors. 6. The relationship between arterial wall [Ca2+] and membrane potential was not significantly different under isobaric (60 mmHg) and non-isobaric conditions (10-100 mmHg), suggesting that intravascular pressure regulates arterial wall [Ca2+] through changes in membrane potential. 7. The results are consistent with the idea that intravascular pressure causes membrane potential depolarization, which opens voltage-dependent Ca2+ channels, acting as 'voltage sensors', thus increasing Ca2+ entry and arterial wall [Ca2+], which leads to vasoconstriction.

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Blood pressure reduction and secondary prevention of stroke and other vascular events: a systematic review.

Philip Bath, Parveen Rashid, Jo Leonardi-Bee (2003)

High blood pressure is a risk factor for stroke recurrence. We assessed the effectiveness of lowering blood pressure in preventing recurrent vascular events in patients with previous stroke or transient ischemic attack. We performed a systematic review and meta-regression of completed randomized controlled trials that investigated the effect of lowering blood pressure on recurrent vascular events in patients with prior ischemic or hemorrhagic stroke or transient ischemic attack. Trials were identified from searches of 3 electronic databases (Cochrane Library, EMBASE, MEDLINE). Seven randomized controlled trials, with 8 comparison groups, were included. Lowering blood pressure or treating hypertension with a variety of antihypertensive agents reduced stroke (odds ratio [OR], 0.76; 95% CI, 0.63 to 0.92), nonfatal stroke (OR, 0.79; 95% CI, 0.65 to 0.95), myocardial infarction (OR, 0.79; 95% CI, 0.63 to 0.98), and total vascular events (OR, 0.79; 95% CI, 0.66 to 0.95). No effect was seen on vascular or all-cause mortality. Heterogeneity was present for several outcomes and was partly related to the class of antihypertensive drugs used; angiotensin-converting enzyme inhibitors and diuretics separately, and especially together, reduced vascular events, while beta-receptor antagonists had no discernable effect. The reduction in stroke was related to the difference in systolic blood pressure between treatment and control groups (P=0.002). Evidence from randomized controlled trials supports the use of antihypertensive agents in lowering blood pressure for the prevention of vascular events in patients with previous stroke or transient ischemic attack. Vascular prevention is associated positively with the magnitude by which blood pressure is reduced.

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Small artery remodeling depends on tissue-type transglutaminase.

Oana Sorop, Erik N. T. P. Bakker, Jop Perree … (2005)

Remodeling of small arteries is essential in the long-term regulation of blood pressure and blood flow to specific organs or tissues. A large part of the change in vessel diameter may occur through non-growth-related reorganization of vessel wall components. The hypothesis was tested that tissue-type transglutaminase (tTG), a cross-linking enzyme, contributes to the inward remodeling of small arteries. The in vivo inward remodeling of rat mesenteric arteries, induced by low blood flow, was attenuated by inhibition of tTG. Rat skeletal muscle arteries expressed tTG, as identified by Western blot and immunostaining. In vitro, activation of these arteries with endothelin-1 resulted in inward remodeling, which was blocked by tTG inhibitors. Small arteries obtained from rats and pigs both showed inward remodeling after exposure to exogenous transglutaminase, which was inhibited by addition of a nitric oxide donor. Enhanced expression of tTG, induced by retinoic acid, increased inward remodeling of porcine coronary arteries kept in organ culture for 3 days. The activity of tTG was dependent on pressure. Inhibition of tTG reversed remodeling, causing a substantial increase in vessel diameter. In a collagen gel contraction assay, tTG determined the compaction of collagen by smooth muscle cells. Collectively, these data show that small artery remodeling associated with chronic vasoconstriction depends on tissue-type transglutaminase. This mechanism may reveal a novel therapeutic target for pathologies associated with inward remodeling of the resistance arteries.

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Author and article information

Journal

Journal ID (publisher-id): JVR

Journal ID (nlm-ta): J Vasc Res

Journal ID (doi): 10.1159/issn.1018-1172

Title: Journal of Vascular Research

Publisher: S. Karger AG

ISSN (Print): 1018-1172

ISSN (Electronic): 1423-0135

Publication date Subscription-year: 2008

Publication date (Print): April 2008

Publication date (Electronic): 14 December 2007

Volume: 45

Issue: 3

Pages: 211-221

Affiliations

Department of Medical Pharmacology and Physiology, Dalton Cardiovascular Research Center, University of Missouri-Columbia, Columbia, Mo., and Department of Systems Biology and Translational Medicine, College of Medicine, Texas A&M University Health Science Center, College Station, Tex., USA

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Publisher ID: 112513 Other ID: J Vasc Res 2008;45:211–221

DOI: 10.1159/000112513

PubMed ID: 18087168

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Persistent Agonist-Induced Vasoconstriction Is Not Required for Angiotensin II to Mediate Inward Remodeling of Isolated Arterioles with Myogenic Tone

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Most cited references 20

Regulation of arterial diameter and wall [Ca2+] in cerebral arteries of rat by membrane potential and intravascular pressure.

Blood pressure reduction and secondary prevention of stroke and other vascular events: a systematic review.

Small artery remodeling depends on tissue-type transglutaminase.

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