Blood Vessels In Hypertension Research Articles

Immunomodulatory Activity of Cytokines in Hypertension: A Vascular Perspective.

Cytokines play a crucial role in the structure and function of blood vessels in hypertension. Hypertension damages blood vessels by mechanisms linked to shear forces, activation of the renin-angiotensin-aldosterone and sympathetic nervous systems, oxidative stress, and a proinflammatory milieu that lead to the generation of neoantigens and damage-associated molecular patterns, ultimately triggering the release of numerous cytokines. Damage-associated molecular patterns are recognized by PRRs (pattern recognition receptors) and activate inflammatory mechanisms in endothelial cells, smooth muscle cells, perivascular nerves, and perivascular adipose tissue. Activated vascular cells also release cytokines and express factors that attract macrophages, dendritic cells, and lymphocytes to the blood vessels. Activated and differentiated T cells into Th1, Th17, and Th22 in secondary lymphoid organs migrate to the vessels, releasing specific cytokines that further contribute to vascular dysfunction and remodeling. This chronic inflammation alters the profile of endothelial and smooth muscle cells, making them dysfunctional. Here, we provide an overview of how cytokines contribute to hypertension by impacting the vasculature. Furthermore, we explore clinical perspectives about the modulation of cytokines as a potential therapeutic intervention to specifically target hypertension-linked vascular dysfunction.

Effect of FEMOKLIM on the state of blood vessels in hypoestrogenemia and arterial hypertension

The article presents the results of duplex scanning of the common carotid arteries (CCA) and assessment of the structural and functional state of the vascular bed of 57 women with arterial hypertension (AH) with hypoestrogenemia. It was found that with hypertension with a reduced level of estradiol, the lumen of the OCA increases, the speed of blood flow in the carotid arteries decreases, which indicates vascular remodeling. In the studied patients, in every third case, an inertial type of vasomotor reaction is detected before treatment, which indicates the contribution of dishormonosis to the progression of hypertension due to the development of endothelial dysfunction. Combined therapy with phytoestrogens and ACE inhibitors improves the structural and functional characteristics of the vascular wall, reduces arterial stiffness. The drug Femoklim is a source of phytohormones, hormones of entomological origin and natural antioxidants, has a positive effect on the state of the vascular system, improves blood microcirculation, is a capillary protector, has a complex harmonizing effect on the body.

Evaluation of the effect of metabolic therapy on the state of blood vessels in estrogen deficiency and hypertension

The article presents the results of duplex scanning of the common carotid arteries (CCA) and assessment of the structural and functional state of the vascular bed women with arterial hypertension (AH) with hypoestrogenemia. It was found that in patients with hypertension with a reduced level of estradiol, there is an expansion of the lumen of the CCA, a decrease in the speed of blood flow in the carotid arteries of a rectilinear course, without hemodynamically significant stenoses, which indicates structural and functional changes in the vascular wall. In the studied patients, in almost every third case, an inertial type of vasomotor reaction is detected before treatment, which indicates the contribution of dishormonosis to the progression of hypertension due to an increase in the stiffness of the vascular wall and the development of endothelial dysfunction. Combination therapy with BioDihydroquercetin and ACE inhibitor improves the structural and functional characteristics of the vascular wall of the CCA, has a positive effect on endothelial dysfunction, reduces the stiffness of the vascular wall of the arteries compared with patients taking ACE inhibitor monotherapy. The drug BioDihydroquercetin, produced with trade mark “Baikal Legend”, is a natural antioxidant, capillaroprotector, strengthens blood vessels, improves blood microcirculation, and is recommended to slow down the aging process of the body.

Regular Black Bean Consumption Is Necessary to Sustain Improvements in Small-Artery Vascular Compliance in the Spontaneously Hypertensive Rat.

Edible legume seeds, such as lentils, have been shown to modulate the structural and functional properties of hypertensive blood vessels, however, the effects of dried beans have not been similarly evaluated. To determine whether beans could attenuate hypertension-induced vascular changes (remodeling and stiffness) in relation to their phytochemical content, spontaneously hypertensive rats (SHR) were fed diets containing black beans (BB; high phytochemical content as indicated by their dark seed coat colour) or navy (white) beans (NB; low phytochemical content) for eight weeks. An additional follow-up phase was included to determine how long the alterations in vascular properties are maintained after bean consumption is halted. Assessments included blood pressure (BP), pulse wave velocity (PWV), vessel compliance (small-artery) and morphology (large-artery), and body composition. Neither BBs nor NBs altered BP or PWV in SHR. SHR-BB demonstrated greater medial strain (which is indicative of greater elasticity) at higher intraluminal pressures (80 and 140 mmHg) compared to SHR-NB. BB consumption for 8 weeks enhanced vascular compliance compared to SHR-NB, as demonstrated by a rightward shift in the stress–strain curve, but this improvement was lost within 2 weeks after halting bean consumption. BB and NB increased lean mass after 8 weeks, but halting BB consumption increased fat mass. In conclusion, regular consumption of BBs may be appropriate as a dietary anti-hypertensive strategy via their positive actions on vascular remodeling and compliance.

Lycium barbarum polysaccharides related RAGE and Aβ levels in the retina of mice with acute ocular hypertension and promote maintenance of blood retinal barrier.

Our previous study verified the protective effects of Lycium barbarum polysaccharides (LBP) on retinal neurons and blood vessels in acute ocular hypertension (AOH) mice. To investigate the effect of LBP on the reactivity of retinal glial cells, an AOH mouse model was established in one eye by maintaining ocular hypertension of 90 mmHg for 60 minutes. Either LBP solution (1 mg/kg) or phosphate-buffered saline was administrated to the mice by gavage daily, starting 7 days before the AOH insult and continuing until the mice were sacrificed for specimen collection on day 4 post-insult. After AOH insult, increased numbers of astrocytes and microglia were observed, together with decreased expression of the following glial cell biomarkers in the retinal ganglion cells of AOH mice: glial fibrillary acidic protein, glutamine synthetase, aquaporin-4, S-100 proteins, ionized calcium-binding adaptor molecule 1, amyloid precursor protein and receptor of advanced glycosylation end-products. After intervention with LBP, the above changes were significantly reduced. Remarkably, morphological remodeling of blood vessel-associated retinal astrocytes, marked by glial fibrillary acidic protein, was also observed. These results, taken together, suggest that LBP regulated the production of amyloid-β and expression of receptor of advanced glycosylation end-products, as well as mediating the activity of retinal glial cells, which may lead to the promotion of better maintenance of the blood-retinal barrier and improved neuronal survival in AOH insult. This study was approved by the Committee for the Use of Live Animals in Teaching and Research (approval No. CULTRA-#1664-08).

Theoretical assessment of the Ca2+ oscillations in the afferent arteriole smooth muscle cell of the rat kidney

The afferent arteriole (AA) of rat kidney exhibits the myogenic response, in which the vessel constricts in response to an elevation in blood pressure and dilates in response to a pressure reduction. Additionally, the AA exhibits spontaneous oscillations in vascular tone at physiological luminal pressures. These time-periodic oscillations stem from the dynamic exchange of Ca[Formula: see text] between the cytosol and the sarcoplasmic reticulum, coupled to the stimulation of Ca[Formula: see text]-activated potassium and chloride channels, and to the modulation of voltage-gated L-type Ca[Formula: see text] channels. The effects of physiological factors, including blood pressure and vasoactive substances, on AA vasomotion remain to be well characterized. In this paper, we analyze a mathematical model of Ca[Formula: see text] signaling in an AA smooth muscle cell. The model represents detailed transmembrane ionic transport, intracellular Ca[Formula: see text] dynamics as well as kinetics of nitric oxide (NO) and superoxide (O[Formula: see text]) formation, diffusion and reaction. NO is an important factor in the maintenance of blood pressure and O[Formula: see text] has been shown to contribute significantly to the functional alternations of blood vessels in hypertension. We perform a bifurcation analysis of the model equations to assess the effect of luminal pressure, NO and O[Formula: see text] on the behaviors of limit cycle oscillations.

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The Roles of Integrins in Mediating the Effects of Mechanical Force and Growth Factors on Blood Vessels in Hypertension

Hypertension is characterized by a sustained increase in vasoconstriction and attenuated vasodilation in the face of elevated mechanical stress in the blood vessel wall. To adapt to the increased stress, the vascular smooth muscle cell and its surrounding environment undergo structural and functional changes known as vascular remodeling. Multiple mechanisms underlie the remodeling process, including increased expression of humoral factors and their receptors as well as adhesion molecules and their receptors, all of which appear to collaborate and interact in the response to pressure elevation. In this review, we focus on the interactions between integrin signaling pathways and the activation of growth factor receptors in the response to the increased mechanical stress experienced by blood vessels in hypertension.

Vascular Oxidative Stress: The Common Link in Hypertensive and Diabetic Vascular Disease

Vascular disease in hypertension and diabetes is associated with increased oxidants. The oxidants arise from NADPH oxidase, xanthine oxidase, and mitochondria. Superoxide anion and hydrogen peroxide are produced by both leukocytes and vascular cells. Nitric oxide is produced in excess by inducible nitric oxide synthase, and the potent oxidant, peroxynitrite, is formed from superoxide and nitric oxide. The damage to proteins caused by oxidants is selective, affecting specific oxidant-sensitive amino acid residues. With some important vascular proteins, for example, endothelial nitric oxide synthase, prostacycline synthase, and superoxide dismutase, oxidation of a single susceptible amino acid inactivates the enzyme. The beneficial effects of antioxidants, at least in animal models of hypertension and diabetes, can in part be ascribed to protection of these and other proteins. Mutant proteins lacking their reactive constituent can recapitulate some disease phenotypes suggesting a pathogenic role of the oxidation. Thus, many of the shared functional abnormalities of hypertensive and diabetic blood vessels may be caused by oxidants. Although studies using antioxidants have failed in patients, the successful treatment of vascular disease with HMG-CoA reductase inhibitors, thromboxane A2 antagonists, and polyphenols may depend on their anti-inflammatory effects and ability to decrease production of damaging oxidants.

Endothelium and Fibrinolysis in Hypertension

Despite the blood vessels in hypertension being exposed to high pressure, the main complications of hypertension (ie, heart attacks and stroke) are paradoxically thrombotic in nature rather than hemorrhagic. Increasing clinical and laboratory evidence is consistent with the concept that hypertension, per se, may confer a prothrombotic or hypercoagulable state, with abnormalities of coagulation, platelets, and the endothelium.1 Indeed, it has long been suggested that the latter organ, with roles in hemostasis and in regulating the NO/endothelin-mediated relaxation and contraction of the blood vessel wall, may be both a target and/or promoter of hypertension and a promoter of thrombosis and, thus, atherosclerosis.2 Other evidence linking the endothelium to atherogenesis is the presence of vasa vasorum in the adventitia and media at a higher density in atherosclerotic tissue, as well as neovascularization and collateral growth bypassing stenotic vascular disease. Such neovascularization reflects the process of angiogenesis, and given these close links, it is no surprise that angiogenesis is yet another important aspect of the pathophysiology of vascular disease, intimately linked with both thrombogenesis and atherogenesis, in a new “vascular triad.”3 For example, the major angiogenic growth factor, vascular endothelial growth factor, is linked with both NO and with a major proinflammatory cytokine, interleukin-6.3 However, skeptics would argue that the clinical (ie, human) evidence does not conclusively show evidence of overt angiogenesis, per se, in conditions such as hypertension, despite (eg) the …

Mechanisms of the Anti-Ischemic Effect of Angiotensin II AT 1 Receptor Antagonists in the Brain

1. Circulating and locally formed Angiotensin II regulates the cerebral circulation through stimulation of AT(1) receptors located in cerebrovascular endothelial cells and in brain centers controlling cerebrovascular flow. 2. The cerebrovascular autoregulation is designed to maintain a constant blood flow to the brain, by vasodilatation when blood pressure decreases and vasoconstriction when blood pressure increases. 3. During hypertension, there is a shift in the cerebrovascular autoregulation to the right, in the direction of higher blood pressures, as a consequence of decreased cerebrovascular compliance resulting from vasoconstriction and pathological growth. In hypertension, when perfusion pressure decreases as a consequence of blockade of a cerebral artery, reduced cerebrovascular compliance results in more frequent and more severe strokes with a larger area of injured tissue. 4. There is a cerebrovascular angiotensinergic overdrive in genetically hypertensive rats, manifested as an increased expression of cerebrovascular AT(1) receptors and increased activity of the brain Angiotensin II system. Excess AT(1) receptor stimulation is a main factor in the cerebrovascular pathological growth and decreased compliance, the alteration of the cerebrovascular eNOS/iNOS ratio, and in the inflammatory reaction characteristic of cerebral blood vessels in genetic hypertension. All these factors increase vulnerability to brain ischemia and stroke. 5. Sustained blockade of AT(1) receptors with peripheral and centrally active AT(1) receptor antagonists (ARBs) reverses the cerebrovascular pathological growth and inflammation, increases cerebrovascular compliance, restores the eNOS/iNOS ratio and decreases cerebrovascular inflammation. These effects result in a reduction of the vulnerability to brain ischemia, revealed, when an experimental stroke is produced, in protection of the blood flow in the zone of penumbra and substantial reduction in neuronal injury. 6. The protection against ischemia resulting is related to inhibition of the Renin-Angiotensin System and not directly related to the decrease in blood pressure produced by these compounds. A similar decrease in blood pressure as a result of the administration of beta-adrenergic receptor and calcium channel blockers does not protect from brain ischemia. 7. In addition, sustained AT(1) receptor inhibition enhances AT(2) receptor expression, associated with increased eNOS activity and NO formation followed by enhanced vasodilatation. Direct AT(1) inhibition and indirect AT(2) receptor stimulation are associated factors normalizing cerebrovascular compliance, reducing cerebrovascular inflammation and decreasing the vulnerability to brain ischemia.8. These results strongly suggest that inhibition of AT(1) receptors should be considered as a preventive therapeutic measure to protect the brain from ischemia, and as a possible novel therapy of inflammatory conditions of the brain.

Endothelium‐Derived Factors in Hypertensive Blood Vessels, Especially Nitric Oxide and Hypertension

AbstractFor Abstract see ChemInform Abstract in Full Text.

Endothelium-derived factors in hypertensive blood vessels, especially nitric oxide and hypertension

Endothelium-dependent relaxation (EDR) in the blood vessels of spontaneously hypertensive rats (SHR) and the role of nitric oxide (NO) in the initiation of hypertension are reviewed. EDR was impaired in blood vessels of SHR depending on age and degree of hypertension when compared with those of normotensive rats. The cause of the impairment varied among the type of blood vessels: a decrease in the production of NO and endothelium-derived relaxing factor (EDRF) and an increase in the production of endothelium-derived contracting factor (EDCF) are the main causes of the impairment in large arteries, while a decrease in endothelium-dependent hyperpolarization and increased release of EDCF are the main causes of the impairment in small arteries. Interactions among these endothelium-derived factors and changes in the interactions are also causes of impairment. Superoxide may be involved in the impairment of EDR by destroying NO. The endothelium depresses smooth muscle contraction, including spontaneous tone developed in vascular smooth muscle, and the depressing effect of the endothelium is impaired in the preparations from SHR. The endothelium of blood vessels of SHR are structurally injured as demonstrated by scanning electron microscopy. Antihypertensive treatment prevented these functional and structural changes. Chronic treatment with inhibitors of NO production in normotensive rats impaired EDR and elevated blood pressure. The impairment of EDR is a secondary change due to continued hypertension, and early initiation of antihypertensive therapy is recommended.

Changes of zero-bending-moment states and structures of rat arteries in response to a step lowering of the blood pressure.

There are many papers on tissue remodeling of blood vessels in hypertension, but there are few documents describing the tissue remodeling of the blood vessels following a step lowering of the blood pressure. The present article presents data on the opening angle, the vessel wall thickness, and the thicknesses of the intima-media and adventitia layers of the blood vessels of the lower body (the abdominal aorta, and the common iliac, femoral, saphenous branch, medial plantar, and plantar metatarsal arteries) of the rat after a step lowering of the blood pressure and flow by a controlled constriction of the aorta below both renal arteries. We found a pattern of changes that depend on space (location on the vascular tree), time (after the blood pressure change), and the intensity of disturbance. We model mathematically the dynamics shown by the experimental results by means of the indicial response functions, which are defined as the morphometric changes in response to a step decrease of blood pressure or blood flow. Under the hypothesis that there is a range of linearity between the degree of tissue remodeling and the amplitude of the pressure change, we can use the indicial functions to predict the remodeling of the vessel under an arbitrary history of decreasing blood pressure; and conversely, we can compute the indicial response functions from pertinent results of a single experiment. The totality of all our experiments is consistent with the linearity hypothesis within the range of the experiment. The mathematical analysis and the formulas are presented in the Appendix.

Involvement of Rho‐kinase in hypertensive vascular disease —a novel therapeutic target in hypertension

Intracellular signaling pathway mediated by Rho/Rho-kinase plays an important role in the regulation of vascular smooth muscle contraction and other cellular functions, including adhesion, migration, proliferation, and hypertrophy. A Rho-kinase inhibitor has been shown to lower blood pressure in hypertensive rats in vivo, however, direct evidence for the involvement of Rho-kinase in hypertensive vascular disease is still lacking. In this study, we tested our hypothesis that Rho-kinase is involved substantially in functional and structural alterations of hypertensive blood vessels in spontaneously hypertensive rats (SHR). Force measurement with isolated blood vessels demonstrated that Rho-kinase was involved significantly in the vascular hyperreactivity in SHR. Biochemical analysis showed that both the expression and the activity of Rho-kinase were augmented in blood vessels of SHR. It is important to note that the involvement of Rho-kinase in the vascular hyperreactivity preceded the development of hypertension. Finally, long-term blockade of Rho-kinase suppressed vascular lesion formation such as medial hepertrophy and perivascular fibrosis in SHR. Our results provide the first evidence that augmented expression and function of Rho-kinase plays a key role in the pathogenesis of hypertensive vascular disease, which suggests that this molecule could be regarded as a novel therapeutic target in hypertension.

Flow cytometric determination of cell proliferation in hypertensive blood vessels.

Measurement of vascular cell proliferation in animal models of hypertension is currently accomplished by demonstrating [(3)H]-thymidine ([(3)H]-dT) incorporation into DNA using autoradiography. This method, however, is labor intensive, requires radioactivity, and is limited by the inherent difficulty in discriminating labeled and unlabeled cells. To address these limitations, a flow cytometric-based method is described utilizing incorporation of 5-bromo-2'-deoxyuridine (BrdU) into DNA of nuclei isolated from blood vessels. Pulmonary hypertension was induced in rats by exposure to 10% O(2) (hypoxia) for varying periods of time. Pulmonary arteries and aorta from rats injected with BrdU prior to sacrifice were isolated, fixed with 10% formalin, and digested with Protease XIV. The intact nuclei liberated by this treatment were successively treated with HCl/Triton X-100 and sodium borate. Processed nuclei were probed with a BrdU-specific fluorescein-conjugated antibody, and the percentage of BrdU staining cells was determined using flow cytometry. An approximately 20-fold increase in BrdU-positive cells at 3 days of hypoxia in pulmonary arteries (relative to control) with no change in aorta was observed. These results were similar to previous studies using [(3)H]-dT labeling. Flow cytometric determination of cell proliferation in blood vessels is a simple, objective technique that may facilitate measurement of cell proliferation in animal models of vascular disease.

Effect of γ-Tocotreenol on Blood Pressure, Lipid Peroxtoation and Total Antioxtoant Status in Spontaneously Hypertensive Rats (SHR)

The aim of this study was to determine the effects of γ tocotrienol on lipid peroxidation and total antioxidant status of spontaneously hypertensive rats (SHR), comparing them with normal Wistar Kyoto (WKY) rats.SHR were divided into three groups and treated with different doses of γ tocotrienol (γl, 15mg/kg diet; γ2, 30mg/kg diet and γ3, 150mg/kg diet). Normal WKY and untreated SHR were used as normal (N) and hypertensive control (HC). Blood pressure were recorded every fortnightly for three months. At the end of the trial, animals were killed and measurement of plasma total antioxidant status, plasma superoxide dismutase (SOD) activity and lipid peroxide levels in plasma and blood vessels were carried out following well established methods.Study shows that lipid peroxides were significantly higher in hypertensive plasma and blood vessels compared to that of normal rats (Plasma- N: 0.06±0.01, HC: 0.13±0.008;

Apoptosis in aorta of deoxycorticosterone acetate-salt hypertensive rats: effect of endothelin receptor antagonism.

Apoptosis or programmed cell death could be greater than normal in various cardiovascular disorders, particularly in the heart. Apoptosis might contribute to remodeling of blood vessels in hypertension and could participate in regulation of vascular hypertrophy/hyperplasia. To investigate apoptosis in deoxycorticosterone acetate (DOCA)-salt hypertension and to determine whether endothelin-1, whose expression is enhanced in these rats, plays a role in apoptosis. We administered two orally active endothelin-A (ET[A])-selective receptor antagonists, A-127,722.5 (30 mg/kg per day) and LU 135,252 (50 mg/kg per day), to establish whether antigrowth effects of these ET(A) antagonists are in part mediated through apoptosis. Apoptosis was evaluated by radiolabeling of 3' OH ends of fragmented DNA, extracted from aortas, using terminal deoxynucleotidyl transferase, to show the presence of internucleosomal DNA splicing as 'DNA laddering'. Its presence was confirmed by in-situ end-labeling. Systolic blood pressure was slightly but significantly lower in treated than it was in untreated DOCA-salt hypertensive rats by a mean of 26 mmHg (P < 0.01) after 4 weeks of treatment with A-127,722.5 and by 19 mmHg (P < 0.01) in rats treated with LU 135,252. Aortic cross-sectional area (CSA) was significantly greater (P < 0.001) in DOCA-salt rats than it was in uninephrectomized controls. This increased CSA was normalized by both ET(A) antagonists. DOCA-salt rats exhibited a greater degree of apoptosis (evaluated by DNA 'laddering') in aorta (353 +/- 14 pixels/microg DNA) than did control rats (232 +/- 10 pixels/microg DNA, P < 0.01). The magnitude of apoptosis was significantly greater (P < 0.01) in aorta of endothelin-antagonist-treated than it was in aorta of untreated DOCA-salt hypertensive rats. In-situ end-labeling confirmed that more apoptosis had occurred in the media of aorta from DOCA-salt hypertensive rats and the further increase found after treatment with the ET(A) antagonists. An increase in apoptosis occurs in aorta of DOCA-salt hypertensive rats, probably as a physiologic counterpart of growth in this hypertensive model. ET(A) antagonists may act in part by accentuating the apoptosis, thereby inducing a blunting of vascular growth, which could also contribute to their antihypertensive effects.

Effect of endothelin antagonism on blood pressure and vascular structure in renovascular hypertensive rats.

To investigate the potential pathogenic role of endothelin in blood pressure elevation and vascular hypertrophy in renovascular hypertensive rats, which present twofold elevations in endothelin-1 mRNA abundance in blood vessels, the response of blood pressure and vascular structure to chronic treatment with the endothelin receptor antagonist bosentan was evaluated. One-kidney, one clip (1K,1C) and two kidney, one clip (2K,1C) Goldblatt hypertensive rats were treated for 2 wk with bosentan (100 mg.kg-1.day-1) in their chow, and systolic blood pressure was measured by the tail-cuff method. Vascular structure was studied in small arteries mounted on a wire myograph. Treatment with bosentan did not result in a significant change in systolic blood pressure or in the structure of small coronary, renal cortical, mesenteric, or femoral arteries in 1K, 1C or in 2K, 1C hypertensive rats. In conclusion, modest (twofold) elevations of endothelin-1 gene expression in blood vessels in renovascular hypertension are not associated with hypotensive responses or regression of vascular hypertrophy during treatment with endothelin antagonists in contrast to what is found in deoxycorticosterone acetate salt hypertensive rats, which exhibit very dramatic increases in endothelin-1 expression (five-to eightfold) and do respond to endothelin antagonism with blood pressure lowering and regression of vascular hypertrophy. These small elevations of vascular endothelin-1 gene expression thus do not appear to indicate the presence of an endothelin component in blood pressure elevation in renovascular hypertension in rats.

Suppression of vascular transforming growth factor-beta1 and extracellular matrix gene expressions by cilazapril and nifedipine in hypertensive rats.

1. We investigated the protective effects of an angiotensin-converting enzyme inhibitor (ACEI) and a Ca antagonist on vascular injury in hypertension. 2. Thirteen week old stroke-prone spontaneously hypertensive rats (SHRSP) were orally given cilazapril (ACEI 10 mg per kg day) or nifedipine (Ca antagonist 30 mg kg per day) for 12 weeks. After the treatment, the aorta and superior mesenteric artery were excised, and subjected to the extraction of RNA. mRNA levels for the transforming growth factor-beta1 (TGF-beta1) and extracellular matrix components such as fibronectin (FN), collagen type I (CoI), type III (CoIII) and type IV (CoIV) and laminin, were measured by northern blot analysis, using each specific cDNA probe. 3. In the mesenteric artery of SHRSP, TGF-beta1 mRNA levels were increased compared with Wistar-Kyoto (WKY) rats, being accompanied by a significant increase in mRNA levels for FN, CoI, CoIII, CoIV and laminin. In the aorta, only TGF-beta1 and fibronectin mRNAs were increased in SHRSP, but collagen and laminin were not increased. 4. Both cilazapril and nifedipine, to similar extents, suppressed the above mentioned increased gene expressions in both mesenteric artery and aorta, being associated with the improvement of vascular hypertrophy. 5. These results suggest that TGF-beta1 may be responsible for smooth muscle cell hypertrophy and the increased deposition of extracellular matrix in hypertensive blood vessels. Both cilazapril and nifedipine may lessen hypertensive vascular thickening, by suppressing the gene expression of TGF-beta1 and extracellular matrix.