Restoration of T-Cell Depression and Suppression of Blood Pressure in Spontaneously Hypertensive Rats (SHR) by Allogeneic Thymus Grafts or Injection of Thymic Hormone

Ba, Denian; Takeichi, Noritoshi; Kobayashi, Hiroshi

doi:10.1536/ihj.22.494

Cited by 62 publications

(79 citation statements)

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“…4 -7 A significant reduction in blood pressure has been observed 6 -14 in SHR with established hypertension given Wistar-King-Aptekman or Wistar thymic implants. This attenuation of hypertension obtained by thymic implantation was dependent on multiple implants, and in one study, 6 this attenuation was transient. However, partial restoration of T cell function was observed in SHR after thymic transplant.…”

Section: Discussionmentioning

confidence: 88%

Interleukin-2 does not attenuate hypertension in spontaneously hypertensive rats.

et al. 1990

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It was recently reported that interleukin-2, when administered as a single bolus injection (5,000 units/kg), could prevent the development of hypertension in young spontaneously hypertensive rats and lower blood pressure to normotensive levels in spontaneously hypertensive rats with established hypertension. Consequently, efforts were made to duplicate this finding. Male spontaneously hypertensive rats (35 days old) were injected subcutaneously with 50,000 units/kg (3,500 units/rat) of recombinant interleukin-2 (Amgen) and had systolic blood pressure measured twice weekly by the tail-cuff technique. Systolic blood pressure in the interleukin-2-treated group was not significantly different from the vehicle-treated control group at any time point over 32 days of follow-up. A second injection of recombinant interleukin-2 (5,000 units/kg) was administered 32 days after the first injection. Again, no reduction in blood pressure was observed in the lnterleukin-2-treated group over an additional 38 days. Mean arterial pressure (±SEM) measured via intra-arterial cannula in conscious rats at age 105 days (38 days after the second treatment) was 168.5±3.5 mm Hg in interleukin-2-treated spontaneously hypertensive rats and 1703±3.6 mm Hg in vehicle-treated controls. Both recombinant interleukin-2 preparations conformed to their respective manufacturer's indicated specific activity as determined by the ability of the interleukin-2 to induce proliferation of the interleukln-2-dependent cell line HT-2. Thus, this study demonstrated that interleukin-2 was ineffective in preventing or attenuating hypertension in spontaneously hypertensive rats. (Hypertension 1990;16:468-471)

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Section: Discussionmentioning

confidence: 88%

Interleukin-2 does not attenuate hypertension in spontaneously hypertensive rats.

et al. 1990

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“…15 -18 Thymus grafts in young SHRs prevent the increase in blood pressure and restore cellular immunological competence. 18 This cellular immunodeficiency could lead to a depressed delayed type of hypersensitivity and allograft rejection. This genetic immunological deficiency may un-derlie the less pronounced allograft rejection in recipient SHRs.…”

Section: Auografts and Isograftsmentioning

confidence: 99%

Allograft-induced arterial wall injury and response in normotensive and spontaneously hypertensive rats.

Plissonnier

Lévy

Salzmann

et al. 1991

Arterioscler Thromb

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The role of genetically determined immune attack and blood pressure in graft rejectioninduced arterial wall injury and response was assessed by studying the compliance and changes in wall structure of aortic isografts and allografts in normotensive (Wistar-Kyoto [WKY]) and hypertensive (spontaneously hypertensive [SHR]) rats. Six groups of 8-week-old rats were compared: sham-operated in both strains, isografts, and allografts between the two strains (SHR aortas grafted in WKYs, designated SWs; WKY aortas grafted in SHRs, designated WSs; isografts in SHRs, designated SSs; and isografts in WKYs, designated WWs). Each arterial graft was studied 8 weeks after transplantation for volume and compliance (pressures of 75-175 mm Hg) under basal conditions. The amounts of collagen, elastin, and nuclei in the media and intima of the walls of control and grafted aortas were quantified morphometrically. Isografts and controls had the same mechanical characteristics under basal conditions: the arterial volume and arterial compliance of hypertensive rats were lower than those of normotensive rats (/?<0.001). Allografts had a greater initial volume (/><0.001) and a lower compliance (p< 0.001) than did isografts. Allografts in SHRs (SSs) were initially dilated, whereas allografted WKYs (WWs) were not There was intimal proliferation in hypertensive isografts (14±0.77 /tin) and in both types of allografts (WS, 69±1.55 /tm; SW, 44±1.81 /tin); nucleus density was higher in hypertensive allografts (WS) than in normotensive allografts (SW); and collagen density was also higher in SW than in WS allografts. Allografts had decreased medial thickness and decreased smooth muscle cell density. Medial thickness and the absolute amounts of elastin and collagen were significantly lower in SWs than in WSs. Rejection of the arterial graft had major effects on arterial wall injury and response in both strains. The thickness and composition of the intimal proliferative response was mainly correlated with the genetically determined blood pressure and smooth muscle cell proliferative potential. In contrast, differences in the medial structural changes of SWs and WSs were correlated mainly with the genetically determined immune process. Functional changes were therefore related to changes in both intimal and medial structure. (Arteriosclerosis and Thrombosis 1991;ll:1690-1699)

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“…4 These investigators and groups led by Strausser, 5 ' 6 Norman, 7 ' 8 and others 9 -10 also reported that modulating the immune system in SHR can to varying extents delay the onset or ameliorate the severity of hypertension. The modulations included treatment with antithymocyte serum, 5 thymus extracts, 11 thymosin fraction 5, 6 thymic implants, 7811 the immunosuppressor agents cyclophosphamide 9 or cyclosporine, 10 and early thymectomy. 12 Although a mechanism relating the dysfunction of T-cell-mediated immunity in SHR to arterial hypertension has not been established, a number of authors 51213 have postulated an autoimmune process in consideration of the evidence of depressed T cell functions and the im-provements observed after early thymectomy or immunosuppression therapy.…”

mentioning

confidence: 99%

Elevation of plasma immunoglobulin A in the spontaneously hypertensive rat.

Chen

Schachter

1993

Hypertension

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Prior studies describe deficiencies of T-cell-mediated immunity in the spontaneously hypertensive rat (SHR) strain of Okamoto and Aoki. This report describes an alteration of humoral immunity: elevation of the plasma concentration of immunoglobulin (Ig) A and of circulating IgA autoantibodies to single-stranded DNA, double-stranded DNA, and thyroglobulin. The increased plasma IgA levels are evident in prehypertensive SHR, hence not secondary to the hypertension, and they result mainly from increments in polymeric IgA. Plasma IgA content also varied concordantly with the level of systolic blood pressure as influenced by age (older>younger) and gender (male>female) in both the SHR and control Wistar-Kyoto rat strains. Strain differences in plasma IgG or IgM were not observed. Studies of peripheral blood lymphocytes indicate that increased production of IgA is one mechanism for the increment in plasma content. The number of blood lymphocytes capable of producing IgA in vitro in response to the mitogen lipopolysaccharide is increased in SHR. When cultured in the absence or presence of lipopolysaccharide, peripheral blood lymphocytes of SHR secrete more IgA in vitro than do cells of the control strain. No significant strain differences in biliary or renal excretion of IgA were observed. The observed alterations of IgA in the SHR either are causative factors in the development of the hypertension or are the products of an epiphenomenon in which IgA and blood pressure are affected separately, but in parallel, by causative factors related to rat strain, age, and gender.

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Restoration of T-Cell Depression and Suppression of Blood Pressure in Spontaneously Hypertensive Rats (SHR) by Allogeneic Thymus Grafts or Injection of Thymic Hormone

Cited by 62 publications

References 0 publications

Interleukin-2 does not attenuate hypertension in spontaneously hypertensive rats.

Interleukin-2 does not attenuate hypertension in spontaneously hypertensive rats.

Allograft-induced arterial wall injury and response in normotensive and spontaneously hypertensive rats.

Elevation of plasma immunoglobulin A in the spontaneously hypertensive rat.

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