The present invention provides, among other things, methods of treating a muscular dystrophy including administering to a subject suffering from or susceptible to a muscular dystrophy an angiotensin (1-7) peptide. The present invention is, in part, based on the unexpected discovery that administration of an angiotensin (1-7) peptide in a muscular dystrophy animal model reduces fibrosis, restores locomotor activity and restores sympathovagal balance, which are characteristic symptoms in patients suffering from muscular dystrophy. Thus, the present invention provides a new and more effective therapy for muscular dystrophy. In some embodiments, an angiotensin (1-7) peptide includes the naturally occurring angiotensin (1-7) amino acid sequence of Asp1-Arg2-Val3-Tyr4-Ile5-His6-Pro7 (SEQID NO:1). In some embodiments, the angiotensin (1-7) peptide is a functional equivalent of SEQ ID NO:1. In some embodiments, the linear peptide has an amino acid sequence of Asp1-Arg2-Val3-Ser4-Ile5-His6-Cys7 (SEQ ID NO:2). In some embodiments, the cyclic peptide is a 4,7-cyclized angiotensin (1-7).

The present invention provides oligopeptides, in particular, Ang-(1-7) derivatives, and methods for using and producing the same. In one particular embodiment, oligopeptides of the invention have higher blood-brain barrier penetration and/or in vivo half-life compared to the native Ang-(1-7), thereby allowing oligopeptides of the invention to be used in a wide variety of clinical applications including in treatment of cognitive dysfunction and/of impairment.

A method for treating a patient suffering from one of septic shock, acute kidney injury, severe hypotension, cardiac arrest, and refractory hypotension, but not from myocardial infarction, is provided. The method includes administering a therapeutically effective dose of Angiotensin II, or Ang II, to the patient.

The present invention provides oligopeptides, in particular, Ang-(1-7) derivatives, and methods for using and producing the same. In one particular embodiment, oligopeptides of the invention have higher blood-brain barrier penetration and/or in vivo half-life compared to the native Ang-(1-7), thereby allowing oligopeptides of the invention to be used in a wide variety of clinical applications including in treatment of cognitive dysfunction and/or traumatic brain injury.

The present invention relates, inter alia, to a method comprising administering to a subject having high output shock and undergoing treatment with a catecholamine at a dose equivalent to at least about 0.2 mcg/kg/min of norepinephrine a dose of angiotensin II which is effective to raise the blood pressure of the subject to a mean arterial pressure (MAP) of about 65 mm Hg or above, and which is effective to reduce the dose of the catecholamine required to maintain a MAP of about 65 mm Hg to the equivalent of about 0.05-0.2 mcg/kg/min norepinephrine or less, or to the equivalent of about 0.05 mcg/kg/min norepinephrine or less.

The present invention is related to the peptide Des-[Asp.sup.1]-[Ala.sup.1]-Angiotensin-(1-7) (Ala.sup.1-Arg.sup.2-Val.sup.3-Tyr.sup.4-Ile.sup.5-His.sup.6-Pro.sup.7) (SEQ ID NO: 1) and/or its related compounds as vasodilating and cardioprotective agents to be used in mammals. This invention also comprises the production of compounds containing Des-[Asp.sup.1]-[Ala.sup.1]-Angiotensin-(1-7) and/or its related compounds and its use in methods for treating and preventing diseases.

A method for treating a patient suffering from one of septic shock, acute kidney injury, severe hypotension, cardiac arrest, and refractory hypotension, but not from myocardial infarction, is provided. The method includes administering a therapeutically effective dose of Angiotensin II, or Ang II, to the patient.

Disclosed here is a method for enhancing synaptogenesis and/or neuritogenesis, reducing neurodegeneration, and/or reducing accumulation or aggregation of Tau proteins in a subject suffering from cochlear synaptopathy or vestibular synaptopathy or a central nervous system disease or condition, comprising administering to said subject in need thereof an effective amount of 2,4-disulfonyl -phenyl tertiary butyl nitrone (2,4-DSPBN) or a pharmaceutically acceptable salt thereof. The method may further comprise administrating N-acetylcysteine (NAC) to the subject.

Disclosed herein is a therapeutic intervention to prevent, reduce, or treat hemodialysis-associated skeletal muscle cramps by administering All receptor agonists or other pharmacologic agents that augment homeostatic responses to hemodialysis while preventing derecruitment of skeletal muscle capillaries.

The present invention provides oligopeptides, in particular, Ang-(1-7) derivatives, and methods for using and producing the same. In one particular embodiment, oligopeptides of the invention have higher blood-brain barrier penetration and/or in vivo half-life compared to the native Ang-(1-7), thereby allowing oligopeptides of the invention to be used in a wide variety of clinical applications including in treatment of cognitive dysfunction and/of impairment.